Immature Stromal Cells Research Articles

Localized cystic disease of the kidney: study of 14 cases and review of the literature.

Localized cystic disease of the kidney (LCDK) is rare without hereditary background and does not progress. It can mimic neoplastic process, leading to unnecessary surgical intervention. We present 14 patients [male-to-female 9:5; mean age 50.3 years (range: 3-79)] with LCDK in a multinational cohort. Flank pain (n=5) and incidental lesions (n=4) were common. All cases were unilateral (9 right, 5 left), and contralateral kidneys were mostly normal (n=11). No family history was present, and none had extrarenal solid organ cysts. Radical and partial nephrectomies were performed in 9 and 5 cases, respectively. All lesionswere multilocular, ranging from 1.8 - 20cm. 2 cases had diffuse renal involvement. Cystic septa contained nonneoplastic elements including renal tubules and glomeruli without primitive epithelial cellular elements, blastema, or immature stromal cells. In addition, we also comprehensively reviewed 75 previously reported cases. Conclusions. LCDK should be considered in the differential of cystic kidney lesions.

Mesangial cell regeneration from exogenous stromal progenitor by utilizing embryonic kidney

Kidney regenerative medicine is expected to be the solution to the shortage of organs for transplantation. In a previous report, we transplanted exogenous renal progenitor cells (RPCs) including nephron progenitor cells (NPCs), stromal progenitor cells (SPCs), and the ureteric bud (UB) into the nephrogenic zone of animal embryos and succeeded in regenerating new nephrons from exogenous NPCs through a fetal developmental program. However, it was unknown whether the renal stromal lineage cells were regenerated from SPCs. The present study aimed to verify the differentiation of SPCs into mesangial cells and renal stromal lineage cells. Here, we found that simply transplanting RPCs, including SPCs, into the nephrogenic zone of wild-type fetal mice was insufficient for differentiation of SPCs. Therefore, to enrich the purity of SPCs, we sorted cells from RPCs by targeting platelet-derived growth factor receptor alpha (PDGFRa) which is a cell surface marker for immature stromal cells and transplanted the PDGFRa-positive sorted cells. As a result, we succeeded in regenerating a large number of mesangial cells and other renal stromal lineage cells including interstitial fibroblasts, vascular pericytes, and juxtaglomerular cells. We have established the method for regeneration of stromal cells from exogenous SPCs that may contribute to various fields, such as regenerative medicine and kidney embryology, and the creation of disease models for renal stromal disorders.

Tissu adipeux et médecine régénératrice

Adipose tissue is abundant and well known for its involvement in obesity and associated metabolic disorders. Its uses in regenerative medicine recently attracted many investigators, as large amounts of this tissue can be easily obtained using liposuction and it contains several populations of immature cells. The largest pool of such cells corresponds to immature stromal cells, called adipose-derived stromal cells (ADSCs). These cells are purified after proteolytic digestion of adipose tissue and selection by an adherent step. ADSCs display many common features with mesenchymal stem cells derived from bone marrow, including paracrine activity, but with some specific features, among which a greater angiogenic potential. This potential is now investigating at clinical level to treat critical ischemic hindlimb by autologous cells. Other potentials are also investigated and the treatment of fistula associated or not with Crohn's disease is reaching now phase III level.

Adipose-derived stromal cells: Their identity and uses in clinical trials, an update

In adults, adipose tissue is abundant and can be easily sampled using liposuction. Largely involved in obesity and associated metabolic disorders, it is now described as a reservoir of immature stromal cells. These cells, called adipose-derived stromal cells (ADSCs) must be distinguished from the crude stromal vascular fraction (SVF) obtained after digestion of adipose tissue. ADSCs share many features with mesenchymal stem cells derived from bone marrow, including paracrine activity, but they also display some specific features, including a greater angiogenic potential. Their angiogenic properties as well as their paracrine activity suggest a putative tumor-promoting role for ADSCs although contradictory data have been published on this issue. Both SVF cells and ADSCs are currently being investigated in clinical trials in several fields (chronic inflammation, ischemic diseases, etc.). Apart from a phase III trial on the treatment of fistula, most of these are in phase I and use autologous cells. In the near future, the end results of these trials should provide a great deal of data on the safety of ADSC use.

A Histologic, Immunohistochemical and Ultrastructural Study of Fibroma, Myofibroblastoma, Leiomyoma and Hemangiopericytoma in Cattle

The immunohistochemical features of tumors from 7 Holstein cows showing fibroblastic, myofibroblastic, smooth muscle or pericytic differentiation are described. In cases 1 and 2, the tumors were characterized by neoplastic fibroblasts immunostained with vimentin alone, but some cells appeared to transiently express alpha smooth muscle actin (SMA) during tumor development. Cutaneous (case 3) and nasal (case 4) myofibroblastomas, which were characterized by SMA and fibronectin positivity, with a minority of cells showing positive reactivity for desmin, were readily distinguishable from tumors of fibroblasts, smooth muscle cells and pericytes by fibronectin staining. The same staining pattern was seen in a vulvar myofibroblastoma (case 5), which differed from a vaginal leiomyoma (case 6) coexpressing SMA and desmin in nearly all neoplastic cells. Both neoplasms, however, had estrogen receptor (ER), and may be derived from immature stromal cells distributed in the vulvovaginal region. A hemangiopericytoma (case 7) resembled myofibroblastomas in cytoskeletal immunophenotypes, but lacked fibronectin. Benign or locally invasive soft tissue tumors with spindle cell morphology and expression of SMA could be divided into several types by immunostaining for SMA, desmin, fibronectin and BR.

Mechanisms of glucocorticoid induced osteoporosis

Glucocorticoid-induced osteoporosis is the most common cause of secondary osteoporosis, and the degree of bone loss is related to the dose of glucocorticoids and the duration of the exposure. However, prolonged exposure to modest doses of glucocorticoids increases the risk of fractures and there is differential individual sensitivity to these steroids. Following treatment with glucocorticoids, there is an initial rapid loss of bone probably due to increased bone resorption and then a slower progressive loss probably secondary to decreased bone remodeling. Glucocorticoids decrease gastrointestinal calcium absorption and enhance bone resorption by increasing osteoclastogenesis since they stimulate the expression of receptor activator of NF-κB ligand and colony stimulating factor-1, and decrease the levels of osteoprotegerin, a soluble decoy receptor for receptor activator of NF-κB ligand. Glucocorticoids may prolong the life of mature osteoclasts under selected conditions. Eventually, glucocorticoids decrease bone remodeling by depleting the population of osteoblasts. This occurs by a decrease in osteoblastogenesis, and an increase in the apoptosis of mature osteoblasts and osteocytes. Glucocorticoids delay the maturation of immature stromal cells toward osteoblasts and inhibit the function of mature osteoblasts. Instead, glucocorticoids enhance adipogenesis, and this probably occurs at the expense of osteoblastic differentiation. The effect is secondary to the induction of CAAT enhancer binding protein beta and CAAT enhancer binding protein delta, and of peroxisome proliferator-activated receptor gamma, which inhibits osteoblastic differentiation. These effects suggest that glucocorticoids play a role in the trade of osteoblasts and adipocytes. This is confirmed further by the fact that Notch is induced by glucocorticoids and Notch inhibits osteoblastogenesis and enhances adipogenesis. Clinically, the early effects of glucocorticoids on bone resorption can be reversed by the administration of bisphosphonates, whereas the inhibitory effects on bone formation might be reversed by parathyroid hormone. In conclusion, glucocorticoids have profound effects on skeletal cells that lead to the development of osteoporosis.

Induction of ossification in the clitoris of neonatal female rats by administration of androgens.

The effects of a single injection of sex steroids in neonatal female Sprague-Dawley rats on the development of os clitoris were studied. Os clitoris was not detected in neonatally intact control female rats at 28 days of age but was seen in 100% of neonatally androgen-injected ovariectomized or nonovariectomized rats at 28 days of age. Testosterone propionate (1 mg) or 5a-dihydrotestosterone (1 mg) was injected sc within 24 h after birth. On the contrary, single injections of progesterone (1 mg) and 17β-estradiol (0.1 mg) in female rats had no effects. Histological studies of the clitoris in female rats treated with testosterone propionate revealed the aggregation of immature stromal cells at 3 days of age, the appearance of homogenous eosinophilic interstitial substance in the intercellular spaces at 7 days of age, the development of hyalin cartilage at 14 days of age, and the formation of bone with cavity at 21 days of age. These results indicate that the initiation of bone formation in the clitoris is ...

新生仔期および幼若期の雄ラットの陰茎骨形成におよぼす男性ホルモンの影響

Osteogenesis in the penial bone was observed in male rat: immature stromal cells of mesenchymal origin appeared in the penis on the 21st day of fetal age and developed to form mature bony structure with the bonemarrow on or before day 7 after birth; the bone was 1.41 +/- 0.12 mm in length. Neonatal castration caused maldevelopment of the penial bone, while prepuberal treatment with testosterone propionate stimulated the bony growth in castrated immature rat. These results suggest that the stromal cells in penile part of newborn male rats have already been destinated to develop into os penis by fetal exposure to androgen and they do not require androgens for further differentiation but for the bony growth after birth.