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Smoothelin
About: Smoothelin is a research topic. Over the lifetime, 264 publications have been published within this topic receiving 14069 citations.
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TL;DR: Two isoforms of a novel smooth muscle cell (SMC) ‐specific cytoskeletal protein, smoothelin, have been described and expression seems to be strictly controlled with respect to cell type and developmental stage and may be related to the mode of contraction of the different cells.
Abstract: Two isoforms of a novel smooth muscle cell (SMC) -specific cytoskeletal protein, smoothelin, have been described. In the adult chick, the 55-kDa smoothelin-A is expressed in visceral SMC, whereas the 120-kDa smoothelin-B is the major product in vascular SMC. Chicken was chosen to study smoothelin expression during embryogenesis and neonatally. Smoothelin-B was found in vascular SMC from stage 20 onward. In visceral SMC, smoothelin-B was present from stage 29 until hatching. Perinatally, a strong up-regulation of smoothelin synthesis was observed in visceral tissues, coinciding with a switch to the A-isoform. Transient smoothelin synthesis was observed in the somites and the developing heart. Western blotting revealed in these tissues a 62-kDa smoothelin isoform, designated smoothelin-C. Expression of the smoothelin isoforms seems to be strictly controlled with respect to cell type and developmental stage and may be related to the mode of contraction of the different cells. © 2001 Wiley-Liss, Inc.
26 citations
TL;DR: The smooth muscle content (as a proportion of the vascular cross-sectional area) of endometrial blood vessels remained unchanged during the normal menstrual cycle and in menorrhagia; however, expression of the VSMC differentiation markers, smoothelin and calponin, was dysregulated in endometrian blood vessels in samples from women with menor rhagia compared with controls.
Abstract: analysed in relation to total number of blood vessels by double immunostaining for endothelial cell markers. main results and the role of chance: Study of VSMC differentiation markers revealed decreased expression of calponin both in aSMA + vessels (P ¼ 0.008) and in relation to total number of vessels (P ¼ 0.001) in late secretory phase endometrium in menorrhagia compared with controls. Smoothelin expression inaSMA + vessels was increased (P ¼ 0.03) in menorrhagia, although this was not significant in relation to the total number of vessels. In normal endometrium, the proportion of blood vessels expressing aSMA increased from 63% in proliferative endometrium to 81% in the late secretory phase (P ¼ 0.002). The overall arterial muscle content did not differ between control and menorrhagia at any phase of the menstrual cycle, occupying 78–81% of gross vascular cross-sectional area during the different menstrual cycle phases. limitations, reasons forcaution: This study included both straight and spiral arterioles and analysed only stratum functionalis. The VSMC differentiation with respect to aSMA expression is an observational study and the data are presented as presence or absence of the differentiation markers in each field of view, corresponding with the vascular cross sections included in the study of vascular muscle content. wider implications of the findings: Smoothelin and calponin have been widely implicated as important regulators of vascular tone, vascular contractility and rate of blood flow. Our results have uncovered a disparate pattern of calponin expression, potentially indicating a dysfunctional contraction mechanism in the endometrial blood vessels in menorrhagia, thus implicating calponin as a potential therapeutic target.
25 citations
TL;DR: Increased expression of smoothelin in patients with detrusor instability and sensory urge implies that the etiology of these dysfunctions includes changes in myogenic parameters, and supports the new classification of the International Continence Society for overactive bladder.
24 citations
TL;DR: Preliminary results suggest global SMTNL1 deletion is associated with greater myogenic reactivity of cerebral arterioles, although the precise mechanism accounting for this finding remains to be defined.
Abstract: Vascular smooth muscle contraction and the myogenic response regulate blood flow in the resistance vascular and contribute to systemic blood pressure. Three pathways are currently known to contribute to the development of the myogenic response: (i) Ca(2+) -dependent phosphorylation of LC20; (ii) Ca(2+) sensitization through inhibition of myosin phosphatase; and (iii) cortical actin polymerization. A number of regulatory smooth muscle proteins are integrated with these pathways to fine tune the response and facilitate adaptations to vascular (patho)physiologies. Of particular interest is the SMTN family of proteins, consisting of SMTN-A, SMTN-B, and the SMTN-like protein, SMTNL1. The SMTN-B and SMTNL1 proteins are both implicated in regulating smooth muscle contractility and contributing to vascular adaptations associated with hypertension, pregnancy, and exercise training. In the case of SMTNL1, the protein plays multiple roles in regulating contraction through functional interactions with contractile regulators as well as transcriptional control of the contractile phenotype and Ca(2+) -sensitizing capacity. For the first time, preliminary results suggest SMTNL1 is involved in the myogenic response of the cerebral resistance vasculature. In this regard, global SMTNL1 deletion is associated with greater myogenic reactivity of cerebral arterioles, although the precise mechanism accounting for this finding remains to be defined.
24 citations
TL;DR: The results indicate that there are distinct functional differences between different EGFR mutations, which argue for the development of mutation specific targeted therapies.
23 citations