ArticleMolecular and cellular biochemistry1994
Alterations in the expression of the beta-cytoplasmic and the gamma-smooth muscle actins in hypertrophied urinary bladder smooth muscle.
Article in Molecular and cellular biochemistry, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 28 citations in OpenAlex.
- De novo ACTA2 mutation causes a novel syndrome of multisystemic smooth muscle dysfunction.American journal of medical genetics. Part A · 2010Article
- Alteration of the PKC-mediated signaling pathway for smooth muscle contraction in obstruction-induced hypertrophy of the urinary bladder.Laboratory investigation; a journal of technical methods and pathology · 2009Article
- Smooth muscle hypertrophy following partial bladder outlet obstruction is associated with overexpression of non-muscle caldesmon.The American journal of pathology · 2004Article
- Characteristics of inflammation-induced hypertrophy of rat intestinal smooth muscle cell.Digestive diseases and sciences · 1999Article
- Targeted expression of SV40 large T-antigen to visceral smooth muscle induces proliferation of contractile smooth muscle cells and results in megacolon.The Journal of biological chemistry · 1999Article
- Transforming growth factor beta1 involvement in the conversion of fibroblasts to smooth muscle cells in the rabbit bladder serosa.The Histochemical journal · 1998Article
- Regulation of actomyosin and contraction in smooth muscle.World journal of urology · 1994Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The obstruction of the bladder outlet induces a marked increase in bladder mass, and this is accompanied by reduced contractility of bladder smooth muscle and alteration in the cellular architecture. In this study, we show that the composition of various isoforms of actin, a major component of the contractile apparatus and the cytoskeletal structure of smooth muscle, is altered in response to the obstruction-induced bladder hypertrophy. Northern blot analysis of the total RNA isolated from hypertrophied urinary bladder muscle, using a cDNA probe specific for smooth muscle gamma-actin, shows over 200% increase in the gamma-actin mRNA. However, the estimate of the amount of actin from the 2D gel reveals only a 16% increase in gamma-actin, since the 2D gel electrophoresis does not distinguish gamma-smooth muscle actin from gamma-cytoplasmic actin. The bladder smooth muscle alpha-actin and the smooth muscle alpha-actin mRNA are not altered in response to the hypertrophy. The obstructed bladder also reveals a decrease in the beta-cytoplasmic actin (37%) and a concomitant diminution in the beta-cytoplasmic actin mRNA (29%). Hence, the composition of the actin isoforms in bladder smooth muscle is altered in response to the obstruction-induced hypertrophy. This alteration of the actin isoforms is observed at both the protein and mRNA levels.
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