Attenuated mesangial cell proliferation related to store-operated Ca2+ entry in aged rat: the role of STIM 1 and Orai 1

Shen, Bing; Zhu, Jiaquan; Zhang, Jin; Jiang, Feifei; Wang, Zhaoyi; Zhang, Yang; Li, Jie; Huang, Dake; Ke, Dao-Ping; Ma, Rong; Du, Juan

doi:10.1007/s11357-013-9511-5

Cited by 17 publications

(17 citation statements)

References 40 publications

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“…Target proteins in the thoracic aorta or mesenteric arteries were examined as previously described . Briefly, proteins were extracted with detergent extraction buffer containing 1% Triton X‐100, 150 mM NaCl, 50 mM Tris‐HCl, 1% sodium deoxycholate, 0.1% SDS, pH 8.0, plus protease inhibitor cocktail tablets and were separated on a 10% SDS‐polyacrylamide gel.…”

Section: Methodsmentioning

confidence: 99%

Increased TRPP2 expression in vascular smooth muscle cells from high‐salt intake hypertensive rats: The crucial role in vascular dysfunction

Zhao

Zhou

et al. 2014

Molecular Nutrition Food Res

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Section: Methodsmentioning

confidence: 99%

Increased TRPP2 expression in vascular smooth muscle cells from high‐salt intake hypertensive rats: The crucial role in vascular dysfunction

Zhao

Zhou

et al. 2014

Molecular Nutrition Food Res

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“… 7 – 9 In advanced aging, the balance of Ca 2+ in cells is gradually lost, which may become a profound factor altering cellular physiological function. 10 – 12 …”

Section: Introductionmentioning

confidence: 99%

“…Our previous study showed that changed SOCE in kidney mesangial cells with aging affected cell proliferation. 12 However, whether SOCE and related vasoconstriction is changed in VSMCs from different vascular beds with aging remains to be determined.…”

Section: Introductionmentioning

confidence: 99%

Contrasting Patterns of Agonist-induced Store-operated Ca2+ Entry and Vasoconstriction in Mesenteric Arteries and Aorta With Aging

Yang

Zhu

Wang

et al. 2015

Journal of Cardiovascular Pharmacology

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Abstract:Ca2+ is a crucial factor in the regulation of smooth muscle contraction. Store-operated Ca2+ entry (SOCE) is one pathway that mediates Ca2+ influx and smooth muscle contraction. Vessel contraction function usually alters with aging to cause severe vascular-related diseases. However, the underlying mechanism is still not fully understood. Here, we assessed intracellular Ca2+ and vessel tension and found that SOCE and SOCE-mediated contraction of vascular smooth muscle cells (VSMCs) was reduced in aorta but increased in mesenteric arteries from aged rats. The results of Western blot and immunofluorescence staining show that the expression levels of Orai1, a store-operated Ca2+ channel, were increased in VSMCs of mesenteric arteries but were reduced in VSMCs of aorta with aging. In conclusion, we demonstrated that the changing pattern of SOCE and SOCE-mediated contraction of VSMCs is completely reversed in mesenteric arteries and aorta with aging, providing a potential therapeutic target for clinical treatment in age-related vascular diseases.

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“…Since TRPC1 is a Ca 2ϩ -permeable channel expressed in kidney cells (10), the results of Niehof and Borlak's study suggest that HNF4␣ may affect diabetic renal changes by regulating renal cell Ca 2ϩ signaling. STIM1-gated Ca 2ϩ channels participate in the Ca 2ϩ response in glomerular MCs (39,42), and dysfunction of MCs contributes to the progression of diabetic kidney disease. Furthermore, the promoter region of Stim1 has a HNF4␣-binding consensus, which was identified by the F-MATCH program (http://www.gene-regulation.com/ cgi-bin/pub/programs/fmatch/ffa2.cgi).…”

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confidence: 99%

Impairment of hepatic nuclear factor-4α binding to theStim1promoter contributes to high glucose-induced upregulation of STIM1 expression in glomerular mesangial cells

Wang

Chaudhari

Ren

et al. 2015

American Journal of Physiology-Renal Physiology

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Wang Y, Chaudhari S, Ren Y, Ma R. Impairment of hepatic nuclear factor 4␣ binding to the Stim1 promoter contributes to high glucoseinduced upregulation of STIM1 expression in glomerular mesangial cells. Am J Physiol Renal Physiol 308: F1135-F1145, 2015. First published March 18, 2015 doi:10.1152/ajprenal.00563.2014.-The present study was carried out to investigate if hepatic nuclear factor (HNF)4␣ contributed to the high glucose-induced increase in stromal interacting molecule (STIM)1 protein abundance in glomerular mesangial cells (MCs). Western blot and immunofluorescence experiments showed HNF4␣ expression in MCs. Knockdown of HNF4␣ using a small interfering RNA approach significantly increased mRNA expression levels of both STIM1 and Orai1 and protein expression levels of STIM1 in cultured human MCs. Consistently, overexpression of HNF4␣ reduced expressed STIM1 protein expression in human embryonic kidney-293 cells. Furthermore, high glucose treatment did not significantly change the abundance of HNF4␣ protein in MCs but significantly attenuated HNF4␣ binding activity to the Stim1 promoter. Moreover, knockdown of HNF4␣ significantly augmented store-operated Ca 2ϩ entry, which is known to be gated by STIM1 and has recently been found to be antifibrotic in MCs. In agreement with those results, knockdown of HNF4␣ significantly attenuated the fibrotic response of high glucose. These results suggest that HNF4␣ negatively regulates STIM1 transcription in MCs. High glucose increases STIM1 expression levels by impairing HNF4␣ binding activity to the Stim1 promoter, which subsequently releases Stim1 transcription from HNF4␣ repression. Since the STIM1-gated storeoperated Ca 2ϩ entry pathway in MCs has an antifibrotic effect, inhibition of HNF4␣ in MCs might be a potential therapeutic option for diabetic kidney disease. hepatic nuclear factor 4␣; stromal interacting molecule 1; storeoperated Ca 2ϩ entry; mesangial cells; high glucose; diabetic nephropathy STORE-OPERATED Ca 2ϩ entry (SOCE) via store-operated Ca 2ϩ channels (SOCs) is a ubiquitous signaling mechanism in both nonexcitable and excitable cells. This Ca 2ϩ signaling regulates diverse cellular functions ranging from cell proliferation and gene expression to cell contraction and secretion (35). Although SOCE was originally described over two decades ago, its molecular mediators were unknown until recently. By high-throughput RNA inhibition screening, two protein families, stromal interacting molecule (STIM) (27, 36) and Orai (13, 48, 59), were identified as required components of SOCE. STIM1 is a single-pass transmembrane protein located primarily in the endoplasmic reticulum (ER) membrane and functions as an ER Ca 2ϩ sensor to sense the ER luminal Ca 2ϩ concentration. Orai1 is a small plasma membrane protein and is believed to be the pore-forming unit of SOCs. Upon depletion of ER Ca 2ϩ , STIM1 aggregates and translocates to ER-plasma membrane junctions, where it physically associates and subsequently activates Orai1 and causes Ca 2ϩ entry into the cytosol (...

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Attenuated mesangial cell proliferation related to store-operated Ca2+ entry in aged rat: the role of STIM 1 and Orai 1

Cited by 17 publications

References 40 publications

Increased TRPP2 expression in vascular smooth muscle cells from high‐salt intake hypertensive rats: The crucial role in vascular dysfunction

Increased TRPP2 expression in vascular smooth muscle cells from high‐salt intake hypertensive rats: The crucial role in vascular dysfunction

Contrasting Patterns of Agonist-induced Store-operated Ca2+ Entry and Vasoconstriction in Mesenteric Arteries and Aorta With Aging

Impairment of hepatic nuclear factor-4α binding to theStim1promoter contributes to high glucose-induced upregulation of STIM1 expression in glomerular mesangial cells

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