Transient receptor potential canonical 6 (TRPC6) and large-conductance Ca-activated K channels (BK), two of the key ion channels for blood filtration function of podocytes, have been implicated in the pathogenesis of kidney diseases. Moreover, it has been reported that miR-200 b plays an important role in regulating the biological processes of podocytes. In this study, we aimed to examine whether there was a relationship between miR-200 b-3p and the two ion channels. It was suggested that miR-200 b-3p down-regulation inhibited the currents of TRPC6 and BK channels. It also showed that miR-200 b-3p inhibition reduced the levels of protein expression and mRNA transcription of TRPC6 and BK channels. Moreover, the down-regulation of miR-200 b-3p resulted in the decrease of the intracellular Ca concentration. It was also suggested that the decrease of BK currents resulting from miR-200 b-3p inhibition could be regulated by TRPC6 channels. TRPC6 blockage also inhibited BK currents and reduced the level of BK expression. These results together suggested that miR-200 b-3p inhibition reduced the currents of TRPC6, which led to the decrease of intracellular Ca concentration. The decrease of Ca source required for BK activation may result in the inhibition of BK currents.
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http://dx.doi.org/10.1016/j.abb.2018.06.013 | DOI Listing |
Cells
December 2024
Department of Biology and Biochemistry, University of Houston, Houston, TX 77204, USA.
Podocytes express large-conductance Ca-activated K channels (BK channels) and at least two different pore-forming KCa1.1 subunit C-terminal splice variants, known as VEDEC and EMVYR, along with auxiliary β and γ subunits. Podocyte KCa1.
View Article and Find Full Text PDFPathol Res Pract
December 2024
Institute for Anatomy and Cell Biology, Saarland University, Homburg, Saar 66421, Germany. Electronic address:
Background: Little is known about the protein expression of the transient receptor potential canonical (TRPC) channels 1, 3, and 6 in the thyroid. Research in human tissue is insufficient. Our aim was to investigate the distribution of TRPC1, 3, and 6 in the healthy human thyroid.
View Article and Find Full Text PDFAnn Anat
December 2024
Saarland University Medical Center (UKS), Department of Gynecology and Obstetrics, Homburg 66424, Germany.
Background: Although to date the pathogenesis of endometriosis remains largely unexplained, it is known that processes of migration, proliferation and revascularization and thus calcium as a messenger substance play an important role. Consecutively, the present study examines the immunohistochemical expression of the calcium transient receptor potential channels 3 and 6 (TRPC3 and TRPC6) in ectopically located (outside the uterine cavity) endometrial tissue.
Methods: Laparoscopically collected and histomorphologically verified endometriosis tissues from several different intraabdominal locations were examined (n = 20) and immunohistochemical stainings were performed with anti-TRPC3 and anti-TRPC6 antibodies (Alomone Labs, Jerusalem).
J Ethnopharmacol
December 2024
Integrative Medicine Research Center, School of Basic Medical Sciences, Guangzhou University of Chinese Medicine, Outer Ring East Road No. 232, Higher Education Mega Center, Guangzhou, 510006, China. Electronic address:
Ethnopharmacological Relevance: Guilu Erxian Jiao (GLEXJ) is a renowned traditional Chinese herbal formula used to tonify the kidney. It is employed to treat psychiatric disorders, and alleviate memory impairment, cognitive dysfunction, and behavioral disorders. Modern pharmacological studies have demonstrated GLEXJ's ability to significantly inhibit the fear response in post-traumatic stress disorder (PTSD) and facilitate the extinction of fear memory.
View Article and Find Full Text PDFInt J Biochem Cell Biol
December 2024
NIHR Respiratory BRC, Department of Respiratory Sciences, University of Leicester, Leicester, UK. Electronic address:
Idiopathic pulmonary fibrosis (IPF) is a severe lung disease affecting around 5 million people globally, with a median survival of 3-4 years. Characterized by excessive scarring of lung tissue, IPF results from the accumulation of myofibroblasts that deposit extracellular matrix (ECM), causing fibrosis. Current treatments, pirfenidone and nintedanib, slow the disease but do not stop its progression.
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