Number Of Vascular Endothelial Cells Research Articles

Repair of the Urethral Mucosa Defect Model Using Adipose-Derived Stem Cell Sheets and Monitoring the Fate of Indocyanine Green-Labeled Sheets by Near Infrared-II.

Treatment of urethral mucosa defects is a major challenge in urology. Synthetic materials or autologous mucosa does not provide satisfactory treatment options for long-term or large urethral mucosa defects. In response to this problem, we used autologous adipose-derived stem cells (ADSCs) to synthesize cell sheets in vitro for repairing urethral mucosa defect models. In order to monitor the localization and distribution of cell sheets in vivo, cells and sheets were labeled with indocyanine green (ICG) and the second near-infrared (NIR-II) fluorescence imaging was performed. ICG-based NIR-II imaging can successfully track ADSCs and sheets in vivo up to 8 W. Then, rabbit urethral mucosa defect models were repaired with ICG-ADSCs sheets. At 3 months after operation, retrograde urethrography showed that ADSC sheets could effectively repair urethral mucosa defect and restore urethral patency. Histological analysis showed that in ADSC sheet groups, continuous epithelial cells covered the urethra at the transplantation site, and a large number of vascular endothelial cells could also be seen. In the cell-free sheet group, there was no continuous epithelial cell coverage at the repair site of the urethra, and the expression of pro-inflammatory factor TNF-α was increased. It shows that the extracellular matrix alone without cells is not suitable for repairing urethral defects. Surviving ADSCs in the sheets may play a key role in the repair process. This study provides a new tracing method for tissue engineering to dynamically track grafts using an NIR-II imaging system. The ADSC sheets can effectively restore the structure and function of the urethra. It provides a new option for the repair of urethral mucosa defects.

Newcastle disease virus expressing an angiogenic inhibitor exerts an enhanced therapeutic efficacy in colon cancer model.

Newcastle disease virus (NDV)-mediated gene therapy is a promising new approach for treatment of cancer but shows limited anti-angiogenesis. VEGF-Trap plays a vital role in anti-angiogenesis. To enhance the anti-tumor effect of NDV, VEGF-Trap gene was incorporated into the genome of rNDV in this study (named rNDV-VEGF-Trap). Results showed that rNDV-VEGF-Trap reduced cell growth ratio by 85.37% and migration ratio by 87.9% in EA.hy926 cells. In vivo studies, rNDV-VEGF-Trap reduced tumor volume and weight of CT26-bearing mice by more than 3 folds. Immunohistochemistry analysis of CD34 showed rNDV-VEGF-Trap significantly decreased the number of vascular endothelial cells in the tumor tissues. Moreover, Western blot analysis demonstrated that treatment with rNDV-VEGF-Trap significantly decreased the phosphorylation levels of AKT, ERK1/2 and STAT3 and increased the expression levels of P53, BAX and cleaved caspase-3 in the tumor tissue. In addition, to evaluate the toxicity of rNDV-VEGF-Trap, serum chemistries were analyzed. The results showed that rNDV-VEGF-Trap caused insignificant changes of creatinine levels, alanine aminotransferase and aspartate transaminase. Furthermore, administration of rNDV-VEGF-Trap did not cause the diarrhoea, decreased appetite, weight decrease and haemorrhage of the experimental mice. These data suggest that rNDV-VEGF-Trap exhibits an enhanced inhibition of CT26-bearing mice by enhancing anti-angiogenesis and apoptosis and may be a potential candidate for carcinoma therapy especially for colon cancer.

Investigating the effects of carvacrol in rats using oxygen-induced retinopathy model.

Purpose:Investigating the effects of intraperitoneal carvacrol administration in rats using the oxygen-induced retinopathy (OIR) model.Methods:A total of 28 newborn Sprague Dawley rats were used and the OIR model was created using the 50/10% oxygen model. The study composed of four groups in total. While the OIR model was not used in Group I (control group), it was created for Groups II, III, and IV. About 0.01 mL carvacrol, bevacizumab, or 0.9% NaCl was administered intraperitoneal (IP) to the rats in all groups on postnatal day (PND) 14 as follows: Group I and Group II were administered 0.9% NaCl, Group III was administered bevacizumab, and Group IV was administered carvacrol. On PND 18, rats were sacrificed and their right eyes were enucleated.Results:Histopathological and immunohistochemical studies showed that the number of vascular endothelial cells (VECs), vascular endothelial growth factor (VEGF), and tumor necrosis factor-α (TNF-α) decreased similarly in Group III and Group IV compared with Group II. VECs values for Group I, Group II, Group III, and Group IV were measured as 0 ± 0, 26.45 ± 4.57, 7.75 ± 1.98, and 5.78 ± 1.72, respectively, and it differed significantly between groups (P < 0.001). Likewise, VEGF levels were observed as 0.06 ± 0.01, 3.31 ± 0.53, 2.47 ± 0.44, and 2.49 ± 0.52, respectively, and it differed significantly between groups (P < 0.001). TNF-α levels were recorded as 0.06 ± 0.01, 3.58 ± 0.38, 2.46 ± 0.49, and 2.29 ± 0.25, respectively, and it differed significantly between groups (P < 0.001). VECs, VEGF, and TNF-α were similar between Group III and IV (range of P values were 0.486–0.998).Conclusion:The study demonstrated that carvacrol significantly reduced retinal pathological angiogenesis, NV, VEC nuclei count, VEGF, and TNF-α levels. Moreover, the observed effects were comparable to those of bevacizumab.

JAK2V617F-Mediated Endothelial Dysfunction Promotes Congestive Heart Failure in a Murine Model of Myeloproliferative Neoplasm

No relevant conflicts of interest to declare.

Chitosan Hydrogel Enhances the Therapeutic Efficacy of Bone Marrow-Derived Mesenchymal Stem Cells for Myocardial Infarction by Alleviating Vascular Endothelial Cell Pyroptosis.

Myocardial infarction (MI) is one of the higher mortality rates, and current treatment can only delay the progression of the disease. Experiments have shown that cell therapy could improve cardiac function and mesenchymal stem cells (MSCs)-based therapies provide a great promising approach in the treatment of MI. However, low cell survival and engraftment restricts the successful application of MSCs for treating MI. Here, we explored whether co-transplantation of a chitosan (CS) thermosensitive hydrogel with bone marrow-derived MSCs (BMSCs) could optimize and maximize the therapeutic of BMSCs in a mouse model of MI. The fate of transplanted BMSCs was monitored by bioluminescence imaging, and the recovery of cardiac function was detected by echocardiogram. Our results proved that CS hydrogel enhanced the BMSCs' survival and the recovery of cardiac function by protecting the vascular endothelial cells. Further studies revealed that the increased number of vascular endothelial cells was due to the fact that transplanted BMSCs inhibited the inflammatory response and alleviated the pyroptosis of vascular endothelial cells. In conclusions, CS hydrogel improved the engraftment of transplanted BMSCs, ameliorated inflammatory responses, and further promoted functional recovery of heart by alleviating vascular endothelial cell pyroptosis.

Regulation of corpus luteum development and maintenance: specific roles of angiogenesis and action of prostaglandin F2a

Development of the corpus luteum (CL) in ruminants occurs in a rapid and time-dependent manner within 1 week after ovulation, with morphologic and biochemical changes in the cells of the theca interna and granulosa cells of the preovulatory follicle. These changes involve luteinisation of steroidogenic cells and angiogenesis to establish normal luteal function (progesterone secretion). The CL is composed of a large number of vascular endothelial cells, large and small steroidogenic luteal cells, smooth muscle cells, pericytes, fibrocytes and immune cells, indicating that the CL is a heterogeneous tissue. Moreover, the CL produces and secretes growth factors (fibroblast growth factor, vascular endothelial growth factor and insulin-like growth factor), vasoactive factors (nitric oxide, angiotensin II and endothelin-1), steroids (progesterone is important for its own production), oxytocin and prostaglandins (PGF2α and PGE2) to regulate luteal formation and development. Clearly, the main function of the CL is to produce progesterone, which is a prerequisite for survival of the embryo, implantation and maintenance of pregnancy. Inadequate luteinisation and angiogenesis during the early luteal phase results in poor progesterone secretion and causes compromised embryo development and reduced fertility. Secretion of adequate amounts of progesterone during luteal development requires "precise luteinisation" of theca and granulosa cells to form luteal cells, neovascularization, and the establishment of a blood supply (angiogenesis). PGF2α in the developing CL acts as a local regulator to enhance progesterone secretion directly and indirectly by stimulating angiogenic factors, VEGF and FGF2. The preceding role of PGF2α may explain why the developing CL does not acquire luteolytic capacity until several days following ovulation. The balance between luteotrophic and luteolytic factors as well as stimulation and inhibition of angiogenic factors during luteal formation, development and maintenance can have a profound effect on the fate of the CL.

Analysis of differential gene expressions of inflammatory and repair-related factors in chronic refractory wounds in clinic

Objective To compare the tissue morphology and gene expressions of inflammatory and repair-related factors in chronic refractory wound tissue including pressure ulcers and diabetic feet. Methods During August 2016 to September 2017, 10 samples of prepuce were collected after circumcision of 10 urological patients [all male, aged (38±4) years old] admitted in the First Affiliated Hospital of Nanchang University and included in normal skin group, samples of tissue around the edge of wounds with blood supply were collected from 9 heat or electric burn patients [6 male patients, 3 female patients, aged (51±8) years old], 13 pressure ulcer patients [9 male patients, 4 female patients, aged (51±14) years old] and 10 diabetic foot patients [8 male patients, 2 female patients, aged (61±10) years old] during the operations. The samples were divided into burn wound group (9 samples), pressure ulcer group (13 samples), and diabetic foot group (10 samples). Ten slices were taken from pressure ulcer group and diabetic foot group respectively, and 5 slices in each group were used to observe the tissue morphology and expressions of Ki67 and CD31 of wounds respectively with immunofluorescence method. Ten samples from normal skin group, 9 samples from burn wound group, 13 samples from pressure ulcer group, and 10 samples from diabetic foot group were collected for analysis of mRNA expressions of vascular endothelial growth factor 192 (VEGF192), transforming growth factor β (TGF-β), vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1) , interleukin-1β (IL-1β), IL-6, and tumor necrosis factor α (TNF-α) by real time fluorescent quantitative reverse transcription polymerase chain reaction. Data were processed with Mann-Whitney U test and Kruskal-Wallis rank-sum test. Results (1) The expression level of Ki67 in diabetic foot group (390±100) was higher than that of pressure ulcer group (182±14, Z=-2.611, P 0.05), while the mRNA expression levels of TGF-β in wounds of pressure ulcer group and diabetic foot group were significantly decreased (H=18.04, 14.50, P 0.05). (4) Compared with those of normal skin group, the mRNA expression levels of VCAM-1 in wounds of burn wound group and pressure ulcer group were significantly increased (H=-22.50, -11.50, P 0.05); the mRNA expression level of ICAM-1 in wounds of burn wound group showed no significant difference (H=-9.50, P>0.05), and the levels of ICAM-1 in wounds of pressure ulcer group and diabetic foot group were significantly decreased (H=16.50, 16.50, P 0.05). (5) Compared with those of normal skin group, except for the mRNA expression level of IL-1β in wounds of diabetic foot group showed no significant difference (H=-10.00, P>0.05), the mRNA expression levels of IL-1β in wounds of burn wound group and pressure ulcer group were significantly increased (H=-32.50, -21.50, P 0.05), the mRNA expression levels of TNF-α in wounds of pressure ulcer group and diabetic foot group were significantly decreased (H=18.04, 14.50, P 0.05). Conclusions The phenotypes of diabetic foot and pressure ulcer vary from the expressions levels of proliferating cell nuclear antigen and blood vessels forming ability to the expression levels of growth factors, cell adhesion factors, and inflammatory cytokines. Key words: Pressure ulcer; Diabetic foot; Cytokines; Gene expression; Chronic refractory wounds

Quercetin Inhibits the Formation of Atherosclerosis Plaque by Protecting Vascular Endothelial Cells

Background: Quercetin and its derivatives are the most widely distributed flavonoids, which have many pharmacological activities, such as anti-oxidation, anti-aging and anti-inflammatory, Quercetin inhibits the occurrence of atherosclerosis (AS) due to its antioxidant activity, but the mechanism is unknown. Results: Our research found that quercetin plays a role in reducing the formation of atherosclerotic plaque by protecting vascular endothelial cell injury. In an atherosclerotic mouse model, quercetin inhibited the formation of atherosclerotic plaques and downregulated the level of endothelial cell protein C receptors (EPCR), thrombomodulin (TM), von willabrand factor (vWF) and intercellular cell adhesion molecule-1(ICAM-1) in peripheral blood of AS mouse, because of increasing the number of vascular endothelial cells at the atherosclerotic plaque. In vitro model of human vascular endothelial cells (HUVECs) injury by H2O2, we found that quercetin significantly reduced endothelial cell apoptosis, and it can prevent vascular endothelial cell injury by inhibiting the secretion of chemokines (CXCL1 and CXCL8) and inflammatory (TNF-α, IL-β, IL-6 and IL-12) factors and reducing macrophage infiltration, at the same time, quercetin promotes the secretion of pro-angiogenic chemokines (CXCL4 and CXCL10) from vascular endothelial cells. Real-time PCR and western-blot assay found that the quercetin protects vascular endothelial cells by inhibiting apoptotic signaling pathway proteins (Bax and Bcl-2) and inflammatory regulatory pathway proteins (IκBα and p65). Conclusion: Consequently, we concluded that the role of quercetin in the protection of vascular endothelial cells against atherosclerotic plaques may be through the inhibition of vascular endothelial cell apoptosis.

Stromal Cell-Derived Growth Factor-1 Alpha-Elastin Like Peptide Fusion Protein Promotes Cell Migration and Revascularization of Experimental Wounds in Diabetic Mice.

Objective: In previous work, we demonstrated the development of a novel fusion protein containing stromal cell-derived growth factor-1 alpha juxtaposed to an elastin-like peptide (SDF1-ELP), which has similar bioactivity, but is more stable in elastase than SDF1. Herein, we compare the ability of a single topical application of SDF1-ELP to that of SDF1 in healing 1 × 1 cm excisional wounds in diabetic mice. Approach: Human Leukemia-60 cells were used to demonstrate the chemotactic potential of SDF1-ELP versus SDF1 in vitro. Human umbilical vascular endothelial cells were used to demonstrate the angiogenic potential of SDF1-ELP versus SDF1 in vitro. The bioactivity of SDF1-ELP versus SDF1 after incubation in ex-vivo diabetic wound fluid was compared. The in-vivo effectiveness of SDF1-ELP versus SDF1 was compared in diabetic mice wound model by monitoring for the number of CD31+ cells in harvested wound tissues. Results: SDF1-ELP promotes the migration of cells and induces vascularization similar to SDF1 in vitro. SDF1-ELP is more stable in wound fluids compared to SDF1. In vivo, SDF1-ELP induced a higher number of vascular endothelial cells (CD31+ cells) compared to SDF1 and other controls, suggesting increased vascularization. Innovation: While growth factors have been shown to improve wound healing, this strategy is largely ineffective in chronic wounds. In this work, we show that SDF1-ELP is a promising agent for the treatment of chronic skin wounds. Conclusion: The superior in vivo performance and stability of SDF1-ELP makes it a promising agent for the treatment of chronic skin wounds.

Association of endothelial progenitor cells and peptic ulcer treatment in patients with type 2 diabetes mellitus.

The present study aimed to investigate the association between endothelial progenitor cells (EPCs) and peptic ulcers in patients with or without type 2 diabetes mellitus (T2DM), in association with the efficiency of peptic ulcer treatment. The study recruited healthy subjects and peptic ulcer patients with or without T2DM. All the ulcer patients, including those with and without T2DM, were administered omeprazole for 8 weeks. Peptic ulcer patients with T2DM were additionally treated with glipizide and novolin. Blood samples were then obtained from the three groups following ulcer treatment. CD133+ cells were isolated from the blood samples using magnetic bead selection, and cultured in complete medium 199. Morphological and quantity changes in EPCs were observed by light and fluorescence microscopy. In addition, flow cytometric analysis was used to quantify the number of vascular endothelial cells. The treatment was partially effective in 7 of the 32 peptic ulcer patients without T2DM and 12 of the 32 peptic ulcer patients with T2DM. However, this treatment was ineffective in 20 of the 32 peptic ulcer patients with T2DM. Notably, 25 peptic ulcer patients without T2DM were defined as completely recovered following treatment. In addition, the number of circulating EPCs as well as their colony forming ability was significantly reduced (P<0.05) in the peptic ulcer patients with T2DM following ulcer treatment, compared with the other groups. Circulating EPC counts were significantly increased in peptic ulcer patients without T2DM, as compared with the healthy controls. With regards to colony formation, peptic ulcer patients without T2DM did not exhibit improved colony formation ability. In conclusion, the number of circulating EPCs and their colony-forming ability was significantly reduced in peptic ulcer patients with T2DM following ulcer treatment when compared with the other groups. This suggests that the poor curative effect of peptic ulcer treatment in these patients is associated with impairment of EPCs.

Effect of intravitreal injection with bevacizumab on expression of integrin-linked kinase in fibrovascular membranes of proliferative diabetic retinopathy

Objective To observe the effect of intravitreal injection of bevacizumab(Avastin,IVB)on the expression of integrin-linked kinase(ILK)in fibrovascular membranes and the number of vascular endothelial cells(VECs)in proliferative diabetic retinopathy(PDR).Methods Twenty-four fibrovascular membrane samples were collected during pars plana vitrectomy in 24 patients with PDR.1 2 PDR patients had received a single 1.25 mg IVB 7 days preoperatively(bevaeizumab group),the other 1 2 patients(nonbevacizumab group)had not received lVB.For each of 24 fibrovascular membranes specimen.the number of VECs in the membranes were counted after staining with hematoxylin-eosin and yon willebrand factor.Expressions of ILK in the fibrovascular membranes were detected through immunohistochemistry analysis.Results Immunohistochemistry revealed that ILK was highly expressed in all of 24 fibrovaseular membranes of PDR.The average optieal density of ILK expression level in bevacizumab and non-bevaeizumab group were(127.78±15.08)and(129.03±16.26)respectively.the difference was not statistically significant (t=0.330,P=0.745).The number of VECs in ftbrovascular membranes in bevacizumab and nonbevaeizumab group were 21.50±3.94 and 41.33±7.44 respectively,the difference was statistically significant(t=3.872,P=0.003).Condusiom ILK was expressed in fibrovascular membranes of PDR.IVB can decrease the number of VECS during the process of PDR,but it can not affect the expression of ILK protein. Key words: Diabetic retinopathy/drug therapy; Antibodies,monoclonal/therapeutic use; Protein kinases; Vascular endothelial growth factors

Tumor-infiltrating CD4+ Th17 cells produce IL-17 in tumor microenvironment and promote tumor progression in human gastric cancer

Recently, a subset of IL-17 producing T cells distinct from Th1 or Th2 cells has been described as key players in inflammation and autoimmune diseases as well as cancer development. In this study, we investigated the expression level of IL-17 and T helper 17 (Th17)-related cytokines in gastric cancer tissues and assessed the association of their expression with angiogenesis and their clinicopathological parameters. Tumor and adjacent normal tissues were obtained from 82 patients with gastric cancer. IL-17, IL-21 and IL-23 mRNA expression levels were quantified by real-time RT-PCR. Th17 infiltration, microvessel density and neutrophil infiltration in tumor tissues were examined by immunohistochemistry and double immunofluorescence histochemistry. Expression of IL-17, IL-21 and IL-23 mRNA was found to be significantly up-regulated in tumor tissues compared with adjacent normal tissues. The expression level of IL-17 mRNA strongly and positively correlated with that of IL-21 mRNA in tumor tissue. The number of vascular endothelial cells and infiltrating neutrophils was significantly larger in tumors expressing a high level of IL-17 mRNA than in tumors expressing a low level of IL-17 mRNA. In tumor tissues most CD4+ cells were stained with anti-IL-17 antibody. The expression level of IL-17 mRNA in gastric tumors was associated with the depth of the tumors, lymph-vascular invasion and lymph node involvement, suggesting that IL-17 obviously was related to tumor progression. IL-17 and IL-21, which regulates IL-17, would be potential therapeutic targets for the treatment of gastric cancer.

Prolongation of Islet Graft Survival Using Concomitant Transplantation of Islets and Vascular Endothelial Cells in Diabetic Rats

Background The transplantation of isolated islets of Langerhans is nearing acceptance as treatment of type 1 diabetes mellitus. Because the arterial and venous connections of the pancreas are disrupted during islet isolation, islets must be revascularized after transplantation. Objective To observe whether increased numbers of vascular endothelial cells in islets can affect the angiogenesis and function of the grafts. Materials and Methods Rats with streptozocin-induced diabetes were divided into 3 groups. The rats in group 1 received islet grafts under the capsule of the left kidney; rats in group 2 received combined vascular endothelial cell and islet transplants; and rats in group 3 served as controls. After the transplantation procedure, blood glucose and insulin concentrations were evaluated daily. Hematoxylin-eosin and immunohistochemical staining was used to detect expression of vascular endothelial growth factor antibodies in the diabetic rat kidneys. The mean microvascular density was also calculated. Results At 3 days posttransplantation, blood glucose and insulin concentrations returned to normal in group 2, however, they declined only slightly in group 1, and moderate hyperglycemia was present. There was a significant difference in blood glucose and insulin concentrations between the 2 groups after 3 days ( P < .05). The mean (SD) microvascular density in group 2 was markedly higher than that in group 1 (12.58 [1.81] vs 10.38 [0.97] P = .04). Conclusion This study suggests that concomitant transplantation of isolated islets with endothelial cells can prolong islet graft survival in diabetic rats.

Clinical and histological findings after intravitreal injection of bevacizumab (Avastin®) in a porcine model of choroidal neovascularization

To examine the effect of intravitreally injected bevacizumab (Avastin) on the histological and angiographic morphology of choroidal neovascularization (CNV) in a masked and placebo-controlled animal study. Choroidal neovascularization was induced surgically in 11 porcine eyes by perforating Bruch's membrane with a retinal perforator. After closure of the ports used for the vitrectomy, which was performed to facilitate the Bruch's membrane rupture, 0.05 ml of either bevacizumab or Ringer-Lactat (placebo) was injected into the vitreous cavity. Eyes were enucleated after 14 days. Fundus photographs and fluorescein angiograms (FAs) were obtained immediately prior to enucleation. Sections of formalin- and paraffin-embedded eyes were examined by light microscopy and by immunohistochemical staining. Placebo-injected eyes exhibited the highest propensity to leak, with five of six eyes leaking on FA, whereas only one of five bevacizumab-injected eyes exhibited leakage. On histological examination, all 11 eyes contained CNV membranes of similar size, regardless of treatment. The number of vascular endothelial cells was significantly reduced (p = 0.03) in CNV membranes from eyes that had been injected with bevacizumab when compared with CNV membranes from placebo-injected eyes. There was a trend towards more retinal pigment epithelium cells (p = 0.16) and fewer glial fibres (p = 0.08) in membranes from bevacizumab-treated eyes compared with placebo-treated eyes. Bevacizumab was identified immunohistochemically in the inner limiting membrane (ILM) and to a lesser degree in the remaining retina. Strong staining was also detected in both retinal blood vessels and entire CNV membranes with no cellular predisposition. Vascular endothelial growth factor expression was found in the CNV membranes, in the ILM, in the ganglion cell layer, in Müller cells throughout the neuroretina and in retinal blood vessels. Bevacizumab significantly reduced the proliferation of vascular endothelial cells in CNV membranes and showed a strong trend towards a reduction of leakage from these membranes. After a single injection, bevacizumab did not exhibit a size reducing effect on CNV, but it was still present in the membranes 14 days after intravitreal injection.

Comparison of fat tissues used in intracordal autologous fat injection

Conclusions: The buccal fat pad appears to be more useful as a source of fat tissues in intracordal fat injection than the abdominal fat tissues used previously. However, further studies are required to confirm this point. Objectives: Fat tissues used in vocal fold augmentation surgery have primarily been harvested from the subcutaneous region of the lower abdomen. It is often difficult to obtain sufficient fat tissue for injection due to the physical features of the individual patient. We have thus adopted a method using fat tissue from the buccal fat pad, which is already used in other plastic surgeries. Methods: This was a retrospective study. We evaluated and compared the histological characteristics of fat cells and the condition of vocal folds after injection of fat tissue extracted from the subcutaneous region of the lower abdomen and from the buccal fat pad. Results: Buccal fat cells were relatively smaller than abdominal fat cells and were not influenced by body mass index (BMI), showing less individual differences according to the physical features of the patient. Numbers of vascular endothelial cells tended to be higher in buccal fat tissues. The percentage of cases showing continuous effects for more than 6 months was slightly higher in cases using buccal fat.

Nitric Oxide and Luteal Blood Flow in the Luteolytic Cascade in the Cow

The corpus luteum (CL) of the estrous cycle in the cow is a dynamic organ which has a lifespan of approximately 17-18 days. The main function of the CL is to produce progesterone (P) that requires for achievement and maintenance of pregnancy. If pregnancy does not occur successfully, the CL must regress within a few days to induce the next chance of ovulation. As the CL matures, the steroidogenic cells establish contact with many capillary vessels, consequently the CL is composed of a large number of vascular endothelial cells that can account for up to 50% of all cells. Therefore, blood vessels and blood flow within the CL have an essential role in luteal function. Nitric oxide (NO), a strong vasorelaxant, is now known to play key roles in a variety of physiological process. Indeed, NO has established itself as a polyvalent molecule which plays a decisive role in regulating multiple functions within female reproductive system. In the CL, NO is produced and regulates luteal blood flow, P secretion and apoptosis of luteal cells as well as endothelial cells. This review describes the current investigation for possible roles of NO in the luteolytic cascade within the bovine CL.

Comparison of fat tissues used in intracordal autologous fat injection

The buccal fat pad appears to be more useful as a source of fat tissues in intracordal fat injection than the abdominal fat tissues used previously. However, further studies are required to confirm this point. Fat tissues used in vocal fold augmentation surgery have primarily been harvested from the subcutaneous region of the lower abdomen. It is often difficult to obtain sufficient fat tissue for injection due to the physical features of the individual patient. We have thus adopted a method using fat tissue from the buccal fat pad, which is already used in other plastic surgeries. This was a retrospective study. We evaluated and compared the histological characteristics of fat cells and the condition of vocal folds after injection of fat tissue extracted from the subcutaneous region of the lower abdomen and from the buccal fat pad. Buccal fat cells were relatively smaller than abdominal fat cells and were not influenced by body mass index (BMI), showing less individual differences according to the physical features of the patient. Numbers of vascular endothelial cells tended to be higher in buccal fat tissues. The percentage of cases showing continuous effects for more than 6 months was slightly higher in cases using buccal fat.

Action of nitric oxide on healthy and inflamed human dental pulp tissue

Irreversible pulpitis has been associated with pain and an increase in the number of pulp inflammatory cells. Based on the action of nitric oxide (NO) elsewhere, NO may possibly participate in the sensory and autonomic innervation of the dental pulp, and may influence local inflammatory responses. The purpose of this study was to analyze normal and inflamed human dental pulp for the presence of NADPH-diaphorase (NADPH-d), as an index of NO system activity. Six non-carious second premolar pulp tissue samples were obtained from young patients who required extractions for orthodontic reasons and six inflamed samples were obtained from symptomatic carious second premolars clinically diagnosed with irreversible pulpitis. Pulp tissue was carefully removed, fixed by immersion in a cold 4% PFA buffered solution for 120 min, rinsed in cold phosphate buffer, and quickly-frozen for cryostat sectioning. Pulp tissue was sectioned perpendicularly to the vertical axis of the tooth at 20 μm and processed for histochemistry. Sections of each specimen were stained with hematoxylin-eosin and other sections were subjected to histochemical NADPH-d detection. Results indicated the presence of NADPH reactivity within the pulps of both normal and carious teeth. In the normal teeth NADPH-d activity was detected in a small number of vascular endothelial cells and fibroblasts. The inflammatory response of the pulp from carious premolars was detected in connective tissue by the presence of an increased number of fibroblasts, angioblasts and collagen fibers. It was possible to determine the extent of odontoblast reactivity since the odontoblast layer was usually absent in these split-peel preparations. There were no obvious signs of stained pulpal nerve fibers. Overall NADPH-d staining was significantly more intense within inflamed pulp tissues compared to normal healthy samples (Mann–Whitney test, p < 0.002). These results suggest that NADPH-d may be used as a marker of inflammatory activity in pulpitis and provide the basis for further studies aiming to clarify the possible functions of NO in human dental pulp in pathophysiological situations.

Local mechanisms for luteolysis in the cow: Novel roles of vasoactive substances in the luteolytic cascade within the corpus luteum

The corpus luteum (CL) in the estrous cycle in the cow is a dynamic organ which has a lifespan of approximately 17–18 days. As the CL matures, the steroidogenic cells establish contact with many capillary vessels and the CL is composed of a large number of vascular endothelial cells that can account for up to 50% of the bovine CL. Furthermore, luteal cells and endothelial cells secrete several vasoactive substances such as prostaglandin F2α (PGF2α), endothelin-1 and angiotensin II. These vasoactive substances also function in regulating progesterone secretion in an autocrine/paracrine manner in the CL. The blood vessels and endothelial cells in the CL therefore have an essential role in the luteal function in the cow. Endometrial PGF2α, the primary luteolysin in the cow, stimulates luteal vasoactive substances during luteolysis. Moreover, luteal vasoactive substances may have key roles in the regulation of luteolysis to induce vasodilatation, vasoconstriction and angiolysis. This review describes the current concept for possible roles of vasoactive substances in the luteolytic cascade within the bovine CL.

Osteoblast-specific Angiopoietin 1 overexpression increases bone mass

Although osteoblasts express the angiogenic protein Angiopoietin 1 (Ang1), the role of Ang1 in bone formation remains largely unknown. Here we report that Ang1 overexpression in osteoblasts driven by the osteoblast-specific 2.3 kb alpha 1 type 1 collagen promoter results in increased bone mass in vivo. In Ang1-transgenic mice (Ang1-Tg), bone volume and bone parameters increased significantly compared with wild-type littermates, although the Ang1 receptor, Tie2 was not expressed in osteoblasts. Tie2 is primarily expressed in vascular endothelial cells, and Ang1-Tie2 signaling is reportedly crucial for angiogenesis. We found that the number of vascular endothelial cells was significantly elevated in Ang1-Tg mice compared with that of wild-type littermates, an increase accompanied by increased alkaline-phosphatase activity, a marker of osteoblast activation. The number of osteoclasts in the bone of Ang1-Tg mice did not differ from wild-type littermates. These results indicate that angiogenesis induced by Ang1 expressed in osteoblasts is coupled with osteogenesis.