Ion Channels in Mesangial Cells: Function, Malfunction, or Fiction

Ma, Rong; Pluznick, Jennifer L.; Sansom, Steven C.

doi:10.1152/physiol.00050.2004

Cited by 36 publications

(43 citation statements)

References 71 publications

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“…Because of the inaccessibility of mesangial cells in vivo, their function and cell biology have been mostly studied after several generations of growth in a culture environment. However, culture condition could change the phenotypes of mesangial cells from those in in vivo environment (15,22). Therefore, the results obtained from cultured HMCs might not necessarily represent physiological presence of TRPCs in this type of cells.…”

Section: Expression Of Trpc Proteinsmentioning

confidence: 99%

“…This process involves both the release of intracellular Ca 2ϩ stores and extracellular Ca 2ϩ entry. The latter occurs via classic, voltage-gated Ca 2ϩ channels, receptor-operated Ca 2ϩ channels, and recently identified store-operated Ca 2ϩ channels in the mesangial cell plasma membrane (22).…”

mentioning

confidence: 99%

“…Although a variety of channels have been described in various mesangial cultures using patch-clamp techniques (22), the majority of channels involved in Ca 2ϩ influx via the plasma membrane have not been defined at the molecular level. These channels include nonselective cation channels, receptor-operated Ca 2ϩ channels, and store-operated Ca 2ϩ channels.…”

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confidence: 99%

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Expression of canonical transient receptor potential (TRPC) proteins in human glomerular mesangial cells

Sours¹,

Du²,

Chu³

et al. 2006

American Journal of Physiology-Renal Physiology

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Mesangial cells are located within glomerular capillary loops and contribute to the physiological regulation of glomerular hemodynamics. The function of mesangial cells is controlled by a variety of ion channels in the plasma membrane, including nonselective cation channels, receptor-operated Ca2+ channels, and recently identified store-operated Ca2+ channels. Although the significance of these channels has been widely acknowledged, their molecular identities are still unknown. Recently, the members of the canonical transient receptor potential (TRPC) protein family have been demonstrated to behave as cation channels. The present study was performed to identify the isoforms of endogenous TRPC proteins in human mesangial cells (HMCs) and their interactions. Western blotting showed that TRPC1, 3, 4, and 6 were expressed in cultured HMCs. Consistently, immunofluorescent confocal microscopy revealed specific stainings for TRPC1, 3, 4, and 6 with predominant intracellular localization. However, TRPC5 and 7 were not detectable at protein level by either Western blotting or immunofluorescent staining. The expression of TRPC1, 3, 4, and 6 was also observed in rat and human glomeruli using fluorescent immunohistochemistry. Furthermore, coimmunoprecipitation experiments and immunofluorescent double staining displayed that TRPC1 had physical interaction with TRPC4 and 6, while no interactions were detected among other isoforms of TRPCs. Ca2+ fluorescent ratiometry measurement showed that store-operated Ca2+ entry in HMCs was significantly reduced by knocking down TRPC1, but enhanced by overexpressing TRPC1. These results suggest that HMCs specifically express isoforms of TRPC1, 3, 4, and 6 proteins. These isoforms of TRPCs might selectively assemble to form functional complexes.

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Section: Expression Of Trpc Proteinsmentioning

confidence: 99%

mentioning

confidence: 99%

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Expression of canonical transient receptor potential (TRPC) proteins in human glomerular mesangial cells

Sours¹,

Du²,

Chu³

et al. 2006

American Journal of Physiology-Renal Physiology

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“…12,13 Like many other cell types, MC function is controlled by intracellular Ca 2+ signals. 11,14 In this regard, store-operated Ca 2+ channel (SOC) plays a pivotal role in many physiologic processes in MCs. 14 SOC is activated on depletion of the endoplasmic reticulum (ER) in response to activation of G protein-coupled receptors.…”

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Store–Operated Ca2+ Channels in Mesangial Cells Inhibit Matrix Protein Expression

Wang

Davis

et al. 2015

Journal of the American Society of Nephrology

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Accumulation of extracellular matrix derived from glomerular mesangial cells is an early feature of diabetic nephropathy. Ca 2+ signals mediated by store-operated Ca 2+ channels regulate protein production in a variety of cell types. The aim of this study was to determine the effect of store-operated Ca 2+ channels in mesangial cells on extracellular matrix protein expression. In cultured human mesangial cells, activation of store-operated Ca 2+ channels by thapsigargin significantly decreased fibronectin protein expression and collagen IV mRNA expression in a dose-dependent manner. Conversely, inhibition of the channels by 2-aminoethyl diphenylborinate significantly increased the expression of fibronectin and collagen IV. Similarly, overexpression of stromal interacting molecule 1 reduced, but knockdown of calcium releaseactivated calcium channel protein 1 (Orai1) increased fibronectin protein expression. Furthermore, 2-aminoethyl diphenylborinate significantly augmented angiotensin II-induced fibronectin protein expression, whereas thapsigargin abrogated high glucose-and TGF-b1-stimulated matrix protein expression. In vivo knockdown of Orai1 in mesangial cells of mice using a targeted nanoparticle siRNA delivery system resulted in increased expression of glomerular fibronectin and collagen IV, and mice showed significant mesangial expansion compared with controls. Similarly, in vivo knockdown of stromal interacting molecule 1 in mesangial cells by recombinant adeno-associated virus-encoded shRNA markedly increased collagen IV protein expression in renal cortex and caused mesangial expansion in rats. These results suggest that store-operated Ca 2+ channels in mesangial cells negatively regulate extracellular matrix protein expression in the kidney, which may serve as an endogenous renoprotective mechanism in diabetes.

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“…Several types of Ca 2ϩ -conductive channels in the plasma membrane are involved in the physiologic processes. These channels include voltage-operated Ca 2ϩ channel (VOCC), receptor-operated channel (ROC), and recently found store-operated channel (SOC) (1,2). In contrast to the widely known VOCC, the molecular identity, physiologic significance, and regulatory mechanism of ROC and SOC in the glomerular contractile cells remain unknown.…”

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Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

Sours-Brothers

Coleman

et al. 2007

Journal of the American Society of Nephrology

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Contractility of mesangial cells (MC) is tightly controlled by [G lomerular mesangial cells (MC) are located within glomerular capillary loops and contribute to the physiologic regulation of glomerular hemodynamics (1). Altered responsiveness of MC to hormones is one of the major causes that lead to various renal diseases. Ca 2ϩ influx across the plasma membrane is a major component of MC responses to vasoconstrictors (1). Several types of Ca 2ϩ -conductive channels in the plasma membrane are involved in the physiologic processes. These channels include voltage-operated Ca 2ϩ channel (VOCC), receptor-operated channel (ROC), and recently found store-operated channel (SOC) (1,2). In contrast to the widely known VOCC, the molecular identity, physiologic significance, and regulatory mechanism of ROC and SOC in the glomerular contractile cells remain unknown.Recently, the channel proteins from a new family, canonical transient receptor potential (TRPC), were found in a variety of cells (3). TRPC family includes seven related members, designated as TRPC1 through 7 (3). Pharmacologic and electrophysiologic studies in conjunction with molecular biologic tools and Ca 2ϩ imagings have demonstrated that TRPC channel activity is tightly linked to the signaling cascade of G protein-coupled receptor or receptor tyrosine kinase (4,5), supporting the current hypothesis that TRPC proteins are potential candidates for ROC and SOC. TRPC proteins have been identified in glomeruli and glomerular MC (6 -8). Our previous work also demonstrated that human MC selectively express TRPC1,3,4, and 6 (9). However, the function, regulation, and physiologic relevance of these glomerular TRPC are unexplored at large extent. In this study, we focused on TRPC1 and investigated its contribution to mesangial contraction in vitro and in vivo. Our results indicate that TRPC1 is an important component mediating contractile responses of MC. The TRPC1-involved mesangial contraction is attributed to TRPC1-associated Ca 2ϩ influx. Materials and Methods AnimalsTwo-to 3-mo-old male Sprague-Dawley rats were used in this study. All rats were purchased from Harlan (Indianapolis, IN). Care and use of all animals in this study were in strict agreement with the guidelines set forth by the University of North Texas Health Science Center. Measurement of GFR and Renal Blood FlowGFR and renal blood flow (RBF) were estimated by measurement of inulin and para-aminohippurate (PAH) plasma clearances as described

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Ion Channels in Mesangial Cells: Function, Malfunction, or Fiction

Cited by 36 publications

References 71 publications

Expression of canonical transient receptor potential (TRPC) proteins in human glomerular mesangial cells

Expression of canonical transient receptor potential (TRPC) proteins in human glomerular mesangial cells

Store–Operated Ca2+ Channels in Mesangial Cells Inhibit Matrix Protein Expression

Canonical Transient Receptor Potential 1 Channel Is Involved in Contractile Function of Glomerular Mesangial Cells

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