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Myocardin and microRNA-1 modulate bladder activity through connexin 43 expression during post-natal development
Journal of cellular physiology, 2013-09, Vol.228 (9), p.1819-1826
Imamura, Masaaki
Sugino, Yoshio
Long, Xiaochun
Slivano, Orazio J.
Nishikawa, Nobuyuki
Yoshimura, Naoki
Miano, Joseph M.
2013
Details
Autor(en) / Beteiligte
Imamura, Masaaki
Sugino, Yoshio
Long, Xiaochun
Slivano, Orazio J.
Nishikawa, Nobuyuki
Yoshimura, Naoki
Miano, Joseph M.
Titel
Myocardin and microRNA-1 modulate bladder activity through connexin 43 expression during post-natal development
Ist Teil von
Journal of cellular physiology, 2013-09, Vol.228 (9), p.1819-1826
Ort / Verlag
Hoboken: Wiley Subscription Services, Inc., A Wiley Company
Erscheinungsjahr
2013
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
Overactive bladder (OAB) is a pervasive clinical problem involving alterations in both neurogenic and myogenic activity. While there has been some progress in understanding neurogenic inputs to OAB, the mechanisms controlling myogenic bladder activity are unclear. We report the involvement of myocardin (MYOCD) and microRNA‐1 (miR‐1) in the regulation of connexin 43 (GJA1), a major gap junction in bladder smooth muscle, and the collective role of these molecules during post‐natal bladder development. Wild‐type (WT) mouse bladders showed normal development from early post‐natal to adult including increases in bladder capacity and maintenance of normal sensitivity to cholinergic agents concurrent with down‐regulation of MYOCD and several smooth muscle cell (SMC) contractile genes. Myocardin heterozygous‐knockout mice exhibited reduced expression of Myocd mRNA and several SMC contractile genes concurrent with bladder SMC hypersensitivity that was mediated by gap junctions. In both cultured rat bladder SMC and in vivo bladders, MYOCD down‐regulated GJA1 expression through miR‐1 up‐regulation. Interestingly, adult myocardin heterozygous‐knockout mice showed normal increases in bladder and body weight but lower bladder capacity compared to WT mice. These results suggest that MYOCD down‐regulates GJA1 expression via miR‐1 up‐regulation, thereby contributing to maintenance of normal sensitivity and development of bladder capacity. J. Cell. Physiol. 228: 1819–1826, 2013. © 2013 Wiley Periodicals, Inc.
Sprache
Englisch
Identifikatoren
ISSN: 0021-9541
eISSN: 1097-4652
DOI: 10.1002/jcp.24333
Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_8157799
Format
–
Schlagworte
Animals
,
Cell Differentiation
,
Cells, Cultured
,
Connexin 43 - genetics
,
Connexin 43 - metabolism
,
Embryonic Development - genetics
,
Embryonic Development - physiology
,
Gene Expression Regulation, Developmental
,
Mice
,
Mice, Knockout
,
MicroRNAs - genetics
,
MicroRNAs - metabolism
,
Muscle Contraction - physiology
,
Myocytes, Smooth Muscle - cytology
,
Myocytes, Smooth Muscle - metabolism
,
Nuclear Proteins - genetics
,
Nuclear Proteins - metabolism
,
Rats
,
Trans-Activators - genetics
,
Trans-Activators - metabolism
,
Up-Regulation
,
Urinary Bladder - metabolism
,
Urinary Bladder - physiology
,
Urinary Bladder, Overactive - metabolism
,
Urinary Bladder, Overactive - physiopathology
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