Rhythmic electrical activity is a feature of most smooth muscles but the mechanical consequences can vary from regular rapid phasic contractions to sustained contracture. For many years it was thought that spontaneous electrical activity originated in smooth muscle cells but recently it has become apparent that there are specialized pacemaker cells in many organs that are morphologically and functionally distinct from smooth muscle and that the former cells are the source of spontaneous electrical activity. Such a pacemaker function is well documented for the ICC of the gastrointestinal tract but evidence is accumulating that ICC-like cells play a similar role in other types of smooth muscle. We have recently shown that there are specialized pacemaking cells in the rabbit urethra which are spontaneously active when freshly isolated, readily distinguishable from smooth muscle cells under bright field illumination and relatively easy to study using patch-clamp and confocal imaging techniques. Recent results suggest that calcium oscillations in isolated rabbit urethral interstitial cells are initiated by calcium release from ryanodine sensitive intracellular stores, that oscillation frequency is very sensitive to the external calcium concentration and that conversion of the primary oscillation to a propagated calcium wave depends upon IP3-induced calcium release.
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http://dx.doi.org/10.1113/jphysiol.2005.098376 | DOI Listing |
Regen Ther
March 2025
Pediatric Urology and Regenerative Medicine Research Center, Gene Cell and Tissue Research Institute Children Medical Center, Tehran University of Medical Sciences, Tehran, Iran.
Tissue engineering has been considered a potential choice for urinary system reconstruction. Here, we aim to a broad spectrum of employed stem cells in bladder regeneration by performing a comprehensive systematic review. In January 2024, we searched Scopus, PubMed, and Embase databases for studies that tried bladder regeneration by tissue engineering using stem cells.
View Article and Find Full Text PDFJVS Vasc Sci
December 2024
Department of Cardiovascular Science, Lewis Katz School of Medicine at Temple University, Philadelphia, PA.
Treatment with an inhibitor of glucose use via glucose transporters (GLUT) has been shown to attenuate experimental abdominal aortic aneurysm (AAA) development in mice. Vascular smooth muscle cell (VSMC) signaling seems to be essential for angiotensin II (Ang II)-induced AAA in mice. Accordingly, we have tested a hypothesis that VSMC silencing of the major GLUT, GLUT1, prevents AAA development and rupture in mice treated with Ang II plus β-aminopropionitrile.
View Article and Find Full Text PDFEClinicalMedicine
January 2025
Department of Mathematics, University of Auckland, Auckland, New Zealand.
With the impending 'retirement' of bronchial thermoplasty (BT) for the treatment of patients with asthma, there is much to learn from this real-world experiment that will help us develop more effective future therapies with the same primary target i.e., airway smooth muscle (ASM) remodelling.
View Article and Find Full Text PDFNat Cardiovasc Res
January 2025
Shanghai Fifth People's Hospital and Institutes of Biomedical Sciences Zhongshan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
Loss-of-function mutations in NOTCH1 were previously linked to thoracic aortopathy, a condition for which non-surgical treatment options are limited. Based on clinical proteome analysis, we hypothesized that mitochondrial fusion and biogenesis in aortic smooth muscle cells (SMCs) are crucial for regulating the progression of NOTCH1-related aortopathy. Here we demonstrate that SMC-specific Notch1 knockout mice develop aortic pathology, including stiffening, dilation and focal dissection.
View Article and Find Full Text PDFNephrol Dial Transplant
January 2025
Division of Nephrology and Section of Mineral Metabolism, Department of Medicine, Heersink School of Medicine, The University of Alabama at Birmingham, Birmingham, AL, USA.
Elevations in systemic phosphate levels, also called hyperphosphatemia, occur in chronic kidney disease (CKD) and during the normal aging process and are associated with various pathologies, such as cardiovascular injury. Experimental studies suggest that at high serum concentrations, phosphate can induce osteogenic differentiation of vascular smooth muscle cells and contribute to vascular calcification. However, the precise underlying mechanism leading to cardiovascular injury is not well understood.
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