Nonpigmented Cells Research Articles

In vivo assay to monitor flavonoid uptake across plant cell membranes

Flavonoids represent one of the most important molecules of plant secondary metabolism, playing many different biochemical and physiological roles. Although their essential role in plant life and human health has been elucidated by many studies, their subcellular transport and accumulation in plant tissues remains unclear. This is due to the absence of a convenient and simple method to monitor their transport. In the present work, we suggest an assay able to follow in vivo transport of quercetin, the most abundant flavonoid in plant tissues. This uptake was monitored using 2-aminoethoxydiphenyl borate (DPBA), a fluorescent probe, in non-pigmented Vitis vinifera cell cultures.

A Case with Pigmented and Non-Pigmented Basal Cell Carcinomas

A Case with Pigmented and Non-Pigmented Basal Cell Carcinomas

Cross-talk between ciliary epithelium and trabecular meshwork cells in-vitro: a new insight into glaucoma.

PurposeIt is assumed that the non-pigmented ciliary epithelium plays a role in regulating intraocular pressure via its neuroendocrine activities. To test this hypothesis, we investigated the effect on a human trabecular meshwork (TM) cell line (NTM) of co-culture with a human non-pigmented ciliary epithelium cell line (ODM-2).MethodsThe cellular cross-talk between ODM-2 and NTM cells was studied in a co-culture system in which the two cell types were co-cultured for 5 to 60min or 2, 4 and 8h and then removed from the co-culture and analyzed. Analyses of the ERK and p38 mitogen-activated protein kinase (MAPK) pathways and of the activity of TM phosphatases and matrix metalloproteins (MMPs) were performed. Acid and alkaline phosphatase activity was determined by the DiFMUP (6, 8-difluoro-4-methylumbelliferyl phosphate) assay. MMP levels were determined by gelatin zymography.ResultsExposure of NTM cells to ODM-2 cells led to the activation of the MAPK signal transduction pathways in NTM cells within 5min of co-culture. Phosphorylation of ERK1/ERK2 and p38 peaked at 10 and 15min and then decreased over time. Interaction between ODM-2 and NTM cells promoted the expression of MMP-9 in the NTM cells after 4h of co-culture.ConclusionsOur findings provide support for the hypothesis that crosstalk does indeed take place between ODM-2 and NTM cells. Future studies should be designed to determine the relationship between the MMP system, MAPK kinases and phosphatases. Manipulation of these signaling molecules and the related NTM signal transduction pathways may provide targets for developing improved treatments for glaucoma.

Human ciliary epithelium as a source of synthesis and secretion of vascular endothelial growth factor in neovascular glaucoma.

Retinal ischemia-induced upregulation of vascular endothelial growth factor (VEGF) leads to endothelial proliferation of the anterior segment, resulting in neovascular glaucoma. To investigate the ciliary epithelium as a possible source of VEGF in human eyes enucleated for intractable neovascular glaucoma. In this proof-of-concept, laboratory-based study, 16 human enucleated eyes (8 with neovascular glaucoma and 8 as controls) were investigated. Presence of VEGF by immunohistochemical analysis (VEGF protein) and in situ hybridization (VEGF messenger RNA). In eyes with neovascular glaucoma, strong VEGF immunoreaction in the nonpigmented epithelial cells of the ciliary processes and in the retina was noted. In situ hybridization for VEGF messenger RNA revealed a similar pattern, with positive stain results only in eyes with neovascular glaucoma. A minimal amount of VEGF immunostaining was seen in control eyes. The nonpigmented ciliary epithelium is an important site of VEGF synthesis in patients with neovascular glaucoma. The ciliary epithelium may represent an additional focus of treatment in the management of neovascular glaucoma, especially in eyes that are nonresponsive to panretinal photocoagulation.

Melatonin receptors trigger cAMP production and inhibit chloride movements in nonpigmented ciliary epithelial cells.

Melatonin and its analog 5-MCA-NAT (5-methylcarboxyamino-N-acetyl tryptamine) are active compounds reducing intraocular pressure (IOP). This action is mediated through MT2 and the putative MT3 melatonin receptor, producing a transient reduction of IOP that lasts for a few hours and has not yet been characterized. The use of melatonin and its analog are causing a decrease in chloride efflux from rabbit nonpigmented epithelial cells (NPE), possibly explaining the decrease in IOP. Melatonin and 5-MCA-NAT inhibited rabbit NPE chloride release in a concentration-dependent manner, whereas the pD2 values were between 4.5 ± 1.2 and 4.4 ± 1.0, respectively. Melatonin hypotensive action was enhanced by the presence of MT2 antagonists, such as DH97 (N-pentanoyl-2-benzyltryptamine) and 4-P-P-DOT (4-phenyl-2-propionamidotetralin) and by the nonselective melatonin receptor antagonist luzindole. Prazosin (1.5 µM) partially reverses the melatonin action by acting as a selective MT3 antagonist. However, at 15 nM it acts as an α-adrenergic receptor antagonist, enhancing the melatonin effect. Regarding the intracellular pathways triggered by melatonin receptors, neither phospholipase C/protein kinase C pathway nor the canonical reduction of intracellular cAMP was responsible for melatonin or 5-MCA-NAT actions. On the contrary, the application of these substances produced a concentration-dependent increase of cAMP, with pD2 values of 4.6 ± 0.2 and 4.9 ± 0.7 for melatonin and 5-MCA-NAT, respectively. In summary, melatonin reduces the release of chloride concomitantly to cAMP generation. The reduction of Cl(-) secretion accounts for a decrease in the water outflow and therefore a decrease in aqueous humor production. This could be one of the main mechanisms responsible for the reduction of IOP after application of melatonin and 5-MCA-NAT.

Abstract 978: microRNA-211 modulates energy metabolism in human melanoma cells by destabilizing HIF1-α and downregulating PDK4

Abstract MicroRNAs (miRNAs) are small noncoding RNAs that play critical roles in cellular physiology and tumorigenesis. We have previously reported that the expression of the melanocyte-specific miRNA miR-211 is significantly reduced or absent in non-pigmented melanoma cells and clinical melanoma samples. Here we report that ectopic expression of miR-211 in non-pigmented melanoma cells increases mitochondrial number, NADP to NADPH ratio, oxygen consumption, and fatty acid synthesis. Ectopic expression of miR-211 destabilizes hypoxia inducible factor 1α (HIF-1α) and downregulates pyruvate dehydrogenase kinase 4 (PDK4), which is known to convert cellular pyruvate to acetyl co-enzyme A. miR-211-expressing cells were characterized by uptake of glutamine, rather than glucose, as a source of cellular energy. Global proteomic, transcriptomic, lipidomic, and metabolomic profiling with integrated analysis revealed that miR-211 modulates several “-omics” signatures associated with oxidative phosphorylation. Here we show for the first time that a microRNA and its target genes play a key role in regulating mitochondrial energy metabolism in melanomas. Citation Format: Joseph Mazar, Adam Richardson, Feng Qi, Bongyong Lee, Angeles Duran, Subramaniam Govindarajan, John Shelley, Laurence M. Brill, Jian-Liang Li, Xianlin Han, Jorge Moscat, Ranjan Joseph Perera. microRNA-211 modulates energy metabolism in human melanoma cells by destabilizing HIF1-α and downregulating PDK4. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 978. doi:10.1158/1538-7445.AM2014-978

Digoxin Derivatives with Enhanced Selectivity for the α2 Isoform of Na,K-ATPase: EFFECTS ON INTRAOCULAR PRESSURE IN RABBITS

In the ciliary epithelium of the eye, the pigmented cells express the α1β1 isoform of Na,K-ATPase, whereas the non-pigmented cells express mainly the α2β3 isoform of Na,K-ATPase. In principle, a Na,K-ATPase inhibitor with selectivity for α2 could effectively reduce intraocular pressure with only minimal local and systemic toxicity. Such an inhibitor could be applied topically provided it was sufficiently permeable via the cornea. Previous experiments with recombinant human α1β1, α2β1, and α3β1 isoforms showed that the classical cardiac glycoside, digoxin, is partially α2-selective and also that the trisdigitoxose moiety is responsible for isoform selectivity. This led to a prediction that modification of the third digitoxose might increase α2 selectivity. A series of perhydro-1,4-oxazepine derivatives of digoxin have been synthesized by periodate oxidation and reductive amination using a variety of R-NH2 substituents. Several derivatives show enhanced selectivity for α2 over α1, close to 8-fold in the best case. Effects of topically applied cardiac glycosides on intraocular pressure in rabbits have been assessed by their ability to either prevent or reverse acute intraocular pressure increases induced by 4-aminopyridine or a selective agonist of the A3 adenosine receptor. Two relatively α2-selective digoxin derivatives efficiently normalize the ocular hypertension, by comparison with digoxin, digoxigenin, or ouabain. This observation is consistent with a major role of α2 in aqueous humor production and suggests that, potentially, α2-selective digoxin derivatives could be of interest as novel drugs for control of intraocular pressure.

Formation and development of rhizoids of the liverwortMarchantia polymorpha1

This paper mainly studies the formation and development of the rhizoids of Marchantia polymorpha L. using light and electron microscopy, and cytochemical methods. Marchantia polymorpha has highly specialized rhizoids that can be divided into two types, namely, tuberculate rhizoids and smooth-walled rhizoids. Tuberculate rhizoids individually originate from the lower superficial cells of the apical meristem. Obvious tubercles exist in the lumen of rhizoids, which always lie parallel to the thallus surface and converge toward the midrib. Smooth-walled rhizoids always exist in clusters in free portions near the midrib in the posterior of the thallus. These smooth rhizoids always grow toward moist soil and lie perpendicular to the thallus surface. Developmental observations show that the initial cell of a tuberculate rhizoid that arises from the lower epidermis possesses a dense cytoplasm. The rapid polar growth of a rhizoid produces a non-pigmented tubular cell. A growing rhizoid possesses an apical cytoplasmic mass, which contains numerous vesicles, Golgi bodies, and peripheral endoplasmic reticula. The nucleus always follows the apical cytoplasmic mass. The remainder of the cytoplasm located behind the nucleus appears to undergo a degeneration process. Simultaneously, a tuberculate wall is formed by the deposition of fibrillar materials onto the inner side of the primary wall. Histochemical investigation shows that the wall of the rhizoid is polysaccharide in nature and most likely contains callose that accounts for their fluorescence property upon staining with Aniline Blue. The base of a smooth-walled rhizoid has small tuberculated projections; however, the wall of the anterior part of the rhizoid is always smooth.

Cutaneous epithelioid melanocytic neurofibroma arising in a patient with neurofibromatosis‐1

Tumors expressing both melanocytic and neural features can pose a diagnostic challenge to the dermatopathologist and provoke questions regarding their lineage. We report a case of a tumor arising on the right cheek of a 9-year-old boy with neurofibromatosis type 1 (NF-1). This neoplasm featured nests of non-pigmented epithelioid cells arising within a neurofibroma. The entire tumor stained strongly with S100, whereas the epithelioid population stained with MART-1, HMB-45 and MiTF. The neoplasm shows only scattered Ki-67 positivity. This tumor represents a neurofibroma with portions that have undergone melanocytic differentiation (melanocytic neurofibroma). This exceedingly rare tumor represents a distinct entity from neurotized melanocytic nevi, combined melanocytic nevi or pigmented neurofibromas and provides further evidence that melanocytes arise indirectly from ventromedial neural crest-derived Schwann cell precursors.

Balloon cell melanoma: a case report with polarized and non-polarized dermatoscopy and dermatopathology

Balloon cell melanoma is a rare melanoma subtype, with only one previous case with dermatoscopy published. It is often non-pigmented, leading to diagnostic difficulty, and there is a tendency for lesions to be thick at diagnosis.We report a case of balloon cell melanoma on the forearm of a 61-year-old man with both polarized and non-polarized dermatoscopy and dermatopathology. It presented as a firm pale nodule with focal eccentric pigmentation. The clinical images evoke a differential diagnosis of dermatofibroma, dermal nevus, Spitz nevus and basal cell carcinoma as well as melanoma. This melanoma was partially pigmented due to a small, pigmented superficial spreading component on the edge of the non-pigmented balloon cell nodule, prompting further evaluation. In retrospect there was the clue to malignancy of polarizing-specific white lines (chrysalis structures) and polymorphous vessels, including a pattern of dot vessels. The reticular lines exclude basal cell carcinoma, polarizing-specific white lines are inconsistent with the diagnosis of dermal nevus and their eccentric location is inconsistent with both Spitz nevus and dermatofibroma. Excision biopsy was performed, revealing a superficial spreading melanoma with two distinct invasive components, one of atypical non-mature epithelioid cells and the other an amelanotic nodular component, comprising more than 50% of the lesion, characterized by markedly distended epithelioid melanocytes showing pseudo-xanthomatous cytoplasmic balloon cell morphology. A diagnosis of balloon cell melanoma, Breslow thickness 1.9 mm, mitotic rate 3 per square millimeter was rendered. Wide local excision was performed, as was sentinel lymph node biopsy, which was negative.

Nonpigmented Ciliary Epithelial Cells Respond to Acetazolamide by a Soluble Adenylyl Cyclase Mechanism

The nonpigmented ciliary epithelium (NPE) is rich in soluble adenylyl cyclase (sAC), a proposed cytoplasmic bicarbonate sensor. Here, we examine the contribution of sAC to an increase in cyclic AMP (cAMP) and changes in a key ion transporter, H(+)-ATPase, in NPE exposed to acetazolamide, a carbonic anhydrase inhibitor (CAI). Cyclic AMP was measured by radioimmunoassay in primary cultured porcine NPE. The pH-sensitive dye BCECF was used to examine cytoplasmic pH regulation. Subcellular protein translocation was examined by Western blot. A transient cAMP increase, detectable within minutes of acetazolamide treatment, was prevented by KH7, a specific sAC inhibitor. Following 10-minute exposure to acetazolamide, the abundance of H(+)-ATPase B1 subunit and sAC was doubled in a plasma membrane-rich fraction, suggesting subcellular translocation. Similar evidence of H(+)-ATPase translocation was observed in NPE exposed to 8-Bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP). Consistent with increased capacity for proton export, acetazolamide increased the rate of pH recovery from acidification. KH7 and bafilomycin A1, an inhibitor of H(+)-ATPase, both prevented the stimulatory effect of acetazolamide on pH recovery. In a parallel study, H(+)-ATPase abundance was found to be higher in the plasma membrane of HEK293 cells that overexpress sAC compared to the normal HEK293 cells. HEK cells that overexpress sAC and had higher H(+)-ATPase abundance displayed a faster rate of pH recovery and greater sensitivity to KH7. Acetazolamide increases cAMP in a response that involves activation of sAC. Subcellular translocation of H(+)-ATPase and an increase in the capacity for proton export by acetazolamide-treated NPE cells is a cAMP-dependent response.

Microfibril-associated glycoprotein-1 controls human ciliary zonule development in vitro.

The ciliary zonule in the eye, also known as Zinn’s zonule, is composed of oxytalan fibers, which are bundles of microfibrils consisting mainly of fibrillin-1. However, it is still unclear which of the microfibril-associated molecules present in the ciliary zonule controls oxytalan fibers. Microfibril-associated glycoprotein-1 (MAGP-1) is the only microfibril-associated molecule identified in the human ciliary zonule. In the present study, we used siRNA against MAGP-1 in cultures of human non-pigmented ciliary epithelial cells to examine the extracellular deposition and appearance of fibrillin-1 employing Western blotting and immunofluorescence. MAGP-1 suppression led to a reduction of fibrillin-1 deposition. Immunofluorescence also confirmed that RNAi-mediated down-regulation of MAGP-1 led to suppression of fiber development. These results suggest that MAGP-1 plays a crucial role in the extracellular deposition of fibrillin-1 during formation of the human ciliary zonule.

Efficacy of Fluorescence Diagnosis-guided Mohs Micrographic Surgery for Pigmented vs Non-pigmented Basal Cell Carcinoma

Pigmented basal cell carcinoma (PBCC) occurs more frequently in Asian population. The efficacy of fluorescence diagnosis (FD) for PBCCs treated with Mohs micrographic surgery has not yet been determined. This study enrolled 255 patients with 258 biopsy-proven BCC lesions: 199 PBCCs (77.1%) and 59 non-PBCCs (22.9%). We compared the clinicopathological and surgical features of the PBCCs and non-PBCCs. Each group was divided into 2 sub-groups, those assessed and not assessed by FD, to retrospectively analyse surgical features. Aggressive histological subtypes were less prevalent in PBCCs than in non-PBCCs. PBCCs required significantly fewer stages of Mohs excision, with significantly smaller surgical margins and surgical depth, than non-PBCCs. FD did not confer any benefits on PBCCs during Mohs micrographic surgery. However, non-PBCCs assessed by FD required significantly fewer Mohs stages, with significantly smaller surgical margins, than lesions not assessed by FD. These findings suggest that FD should be performed before Mohs micrographic surgery to delineate the margins of non-PBCCs in Asians.

Nonselective Assembly of Fibrillin 1 and Fibrillin 2 in the Rodent Ocular Zonule and in Cultured Cells: Implications for Marfan Syndrome

Fibrillins are the major constituent of tissue microfibrils, which form the ocular zonule. In Marfan syndrome (MFS), FBN1 mutations lead to ectopia lentis. The goal of this work was to investigate zonule composition and formation in fibrillin-deficient and wild-type mice. Immunofluorescence staining of eyes from wild-type, Fbn1-deficient, and Fbn2-deficient mice, as well as other species, was performed using monospecific fibrillin 1 and fibrillin 2 antibodies. The zonule of Fbn1-deficient and Fbn2-deficient mice was studied by electron microscopy. Microfibril formation in vitro was evaluated by immunofluorescence microscopy of cultured nonpigmented ciliary epithelial cells and fibroblasts. A zonule was present in both Fbn1-deficient and Fbn2-deficient mouse eyes. Immunofluorescence demonstrated that the zonule of Fbn1-deficient mice, wild-type mice, rats, and hamsters contained fibrillin 2. The zonule of Fbn2(-/-) mice contained fibrillin 1. Fibrillin 1 and fibrillin 2 colocalized in microfibrils formed in human nonpigmented ciliary epithelium cultures. Like fibrillin 1, fibrillin 2 microfibril assembly was fibronectin dependent and initiated by cell surface punctate deposits that elongated to form microfibrils. These data suggest that fibrillin 1 assembly and fibrillin 2 assembly share similar mechanisms. Microfibril composition depends substantially on the local levels of fibrillin isoforms and is not highly selective in regard to the isoform. This raises the intriguing possibility that the zonule could be strengthened in MFS by inducing fibrillin 2 expression in ciliary epithelium. The presence of fibrillin 2 in the murine zonule and an intact zonule in Fbn1-knockout mice may limit the utility of rodent models for studying ectopia lentis in MFS.

Nodal Combined Blue Nevus and Benign Nevus Cells in Multiple Axillary Sentinel Nodes in a Patient With Breast Carcinoma

Combined blue nevus and benign nevus cells were identified in the same sentinel lymph node. Blue nevus alone was also present in an additional sentinel lymph node in the same axilla in a patient who underwent needle localization, wide local excision, and sentinel lymph node biopsy for her pT1cN1mi(sn)M(na) invasive duct carcinoma of the breast. Of the 4 sentinel lymph nodes, 1 showed micrometastasis and 2 other lymph nodes showed blue nevus involving the capsule and trabeculae of the nodes. The patient had no significant previous clinical history of any skin tumors and had a negative clinical examination for malignant melanoma or pigmented skin lesions after the diagnosis of nodal blue nevus. To our knowledge, this is the first case report of combined blue nevi involving multiple sentinel lymph nodes in the same axilla. An equally interesting finding is the presence of benign nonpigmented nevus cells in continuation with the blue nevus in the same node.

Involvement of AP-1 and C/EBPβ in Upregulation of Endothelin B (ETB) Receptor Expression in a Rodent Model of Glaucoma

Previous studies showed that the endothelin B receptor (ETB) expression was upregulated and played a key role in neurodegeneration in rodent models of glaucoma. However, the mechanisms underlying upregulation of ETB receptor expression remain largely unknown. Using promoter-reporter assays, the 1258 bp upstream the human ETB promoter region was found to be essential for constitutive expression of ETB receptor gene in human non-pigmented ciliary epithelial cells (HNPE). The −300 to −1 bp and −1258 to −600 bp upstream promoter regions of the ETB receptor appeared to be the key binding regions for transcription factors. In addition, the crucial AP-1 binding site located at −615 to −624 bp upstream promoter was confirmed by luciferase assays and CHIP assays which were performed following overexpression of c-Jun in HNPE cells. Overexpression of either c-Jun or C/EBPβ enhanced the ETB receptor promoter activity, which was reflected in increased mRNA and protein levels of ETB receptor. Furthermore, knock-down of either c-Jun or C/EBPβ in HNPE cells was significantly correlated to decreased mRNA levels of both ETB and ETA receptor. These observations suggest that c-Jun and C/EBPβ are important for regulated expression of the ETB receptor in HNPE cells. In separate experiments, intraocular pressure (IOP) was elevated in one eye of Brown Norway rats while the corresponding contralateral eye served as control. Two weeks of IOP elevation produced increased expression of c-Jun and C/EBPβ in the retinal ganglion cell (RGC) layer from IOP-elevated eyes. The mRNA levels of c-Jun, ETA and ETB receptor were upregulated by 2.2-, 3.1- and 4.4-fold in RGC layers obtained by laser capture microdissection from retinas of eyes with elevated IOP, compared to those from contralateral eyes. Taken together, these data suggest that transcription factor AP-1 plays a key role in elevation of ETB receptor in a rodent model of ocular hypertension.

Piceatannol suppresses endotoxin-induced ocular inflammation in rats.

Anti-inflammatory effect of piceatannol, a naturally occurring polyphenol and a potent free radical scavenger, on ocular inflammation is not known. We examined the anti-inflammatory role of piceatannol in ocular inflammatory response due to endotoxin-induced uveitis (EIU) in rats. EIU was induced in Lewis rats by subcutaneous injection of lipopolysaccharide (LPS; 150 ug/rat). Piceatannol (30mg/kg body wt, i.p) was injected either 2h prior to or 1h post LPS induction. A significant increase in the number of infiltrating cells, total protein, and various cytokines and chemokines in AqH were observed in the EIU rat eyes as compared to control groups. However, pre- or post-treatment of piceatannol significantly blocked the LPS-induced changes. Further, piceatannol also suppressed the expression of cyclooxygenase-2 (Cox-2), inducible nitric oxide synthase (iNOS) and activation of NF-κB in the ciliary bodies as well as retina. Further, piceatannol also inhibited the expression of Cox-2, iNOS, and phosphorylation of NF-κB in primary human non-pigmented ciliary epithelial cells (HNPECs) treated with LPS. Similarly, piceatannol also diminished LPS-induced level of NO and prostaglandin E2 in HNPECs. Thus our results demonstrate an anti-inflammatory role of piceatannol in suppressing ocular inflammation induced by endotoxin in rats.

DIDS inhibits Na-K-ATPase activity in porcine nonpigmented ciliary epithelial cells by a Src family kinase-dependent mechanism

The anion transport inhibitor DIDS is known to reduce aqueous humor secretion but questions remain about anion dependence of the effect. In some tissues, DIDS is reported to cause Na-K-ATPase inhibition. Here, we report on the ability of DIDS to inhibit Na-K-ATPase activity in nonpigmented ciliary epithelium (NPE) and investigate the underlying mechanism. Porcine NPE cells were cultured to confluence on permeable supports, treated with drugs added to both sides of the membrane, and then used for (86)Rb uptake measurements or homogenized to measure Na-K-ATPase activity or to detect protein phosphorylation. DIDS inhibited ouabain-sensitive (86)Rb uptake, activated Src family kinase (SFK), and caused a reduction of Na-K-ATPase activity. PP2, an SFK inhibitor, prevented the DIDS responses. In BCECF-loaded NPE, DIDS was found to reduce cytoplasmic pH (pHi). PP2-sensitive Na-K-ATPase activity inhibition, (86)Rb uptake suppression, and SFK activation were observed when a similar reduction of pHi was imposed by low-pH medium or an ammonium chloride withdrawal maneuver. PP2 and the ERK inhibitor U0126 prevented robust ERK1/2 activation in cells exposed to DIDS or subjected to pHi reduction, but U0126 did not prevent SFK activation or the Na-K-ATPase activity response. The evidence points to an inhibitory influence of DIDS on NPE Na-K-ATPase activity by a mechanism that hinges on SFK activation associated with a reduction of cytoplasmic pH.

DIDS and the Janus-faced Na+-K+-activated ATPase. Focus on “DIDS inhibits Na-K-ATPase activity in porcine nonpigmented ciliary epithelial cells by a Src family kinase-dependent mechanism”

the maintenance of mammalian cell volume fundamentally rests on net cation extrusion through Na+-K+-activated ATPase, the Na+ pump. The publication by Shahidullah et al. ([11][1]) persuasively identifies the series of events by which a widely used inhibitor of anion transport, DIDS, can reduce Na+

Morphogenetic Model for Radial Streaking in the Fundus of the Carrier State of X-Linked Albinism

Morphogenetic Model for Radial Streaking in the Fundus of the Carrier State of X-Linked Albinism