ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Targeted STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 48 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
48 citing papers in PubMed, 78 citations in OpenAlex.
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- Orai channel pharmacological manipulation reduces metabolic flexibility in cardiac fibroblasts.American journal of physiology. Cell physiology · 2025Article
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- Calcineurin Is a Universal Regulator of Vessel Function-Focus on Vascular Smooth Muscle Cells.Cells · 2023Review
- Upregulation of Orai Channels Contributes to Aging-Related Vascular Alterations in Rat Coronary Arteries.International journal of molecular sciences · 2023Article
- Familial 4p Interstitial Deletion Provides New Insights and Candidate Genes Underlying This Rare Condition.Genes · 2023Article
- Overcoming Confounding to Characterize the Effects of Calcium Channel Blockers.Function (Oxford, England) · 2023Article
- Salivary gland function, development, and regeneration.Physiological reviews · 2022Review
- STIM1 is a core trigger of airway smooth muscle remodeling and hyperresponsiveness in asthma.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- STIM and Orai Mediated Regulation of Calcium Signaling in Age-Related Diseases.Frontiers in aging · 2022Review
- [Pt(O,O'-acac)(γ-acac)(DMS)]: Alternative Strategies to Overcome Cisplatin-Induced Side Effects and Resistance in T98G Glioma Cells.Cellular and molecular neurobiology · 2021Article
- ORAI1 CaFrontiers in cell and developmental biology · 2021Review
- Store-Operated Calcium Entry in the Cardiovascular System.Advances in experimental medicine and biology · 2021Review
- Role of NFAT in the Progression of Diabetic Atherosclerosis.Frontiers in cardiovascular medicine · 2021Review
- Mechanism of contractile dysfunction induced by serotonin in coronary artery in spontaneously hypertensive rats.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
- L-type CaProceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
Abstract
The Ca(2+)-sensing stromal interaction molecule (STIM) proteins are crucial Ca(2+) signal coordinators. Cre-lox technology was used to generate smooth muscle (sm)-targeted STIM1-, STIM2-, and double STIM1/STIM2-knockout (KO) mouse models, which reveal the essential role of STIM proteins in Ca(2+) homeostasis and their crucial role in controlling function, growth, and development of smooth muscle cells (SMCs). Compared to Cre(+/-) littermates, sm-STIM1-KO mice showed high mortality (50% by 30 d) and reduced bodyweight. While sm-STIM2-KO was without detectable phenotype, the STIM1/STIM double-KO was perinatally lethal, revealing an essential role of STIM1 partially rescued by STIM2. Vascular and intestinal smooth muscle tissues from sm-STIM1-KO mice developed abnormally with distended, thinned morphology. While depolarization-induced aortic contraction was unchanged in sm-STIM1-KO mice, α1-adrenergic-mediated contraction was 26% reduced, and store-dependent contraction almost eliminated. Neointimal formation induced by carotid artery ligation was suppressed by 54%, and in vitro PDGF-induced proliferation was greatly reduced (79%) in sm-STIM1-KO. Notably, the Ca(2+) store-refilling rate in STIM1-KO SMCs was substantially reduced, and sustained PDGF-induced Ca(2+) entry was abolished. This defective Ca(2+) homeostasis prevents PDGF-induced NFAT activation in both contractile and proliferating SMCs. We conclude that STIM1-regulated Ca(2+) homeostasis is crucial for NFAT-mediated transcriptional control required for induction of SMC proliferation, development, and growth responses to injury.-Mancarella, S., Potireddy, S., Wang, Y., Gao, H., Gandhirajan, K., Autieri, M., Scalia, R., Cheng, Z., Wang, H., Madesh, M., Houser, S. R., Gill, D. L. Targeted STIM deletion impairs calcium homeostasis, NFAT activation, and growth of smooth muscle.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.