Phenotypic changes in the regenerating rabbit bladder muscle. Role of interstitial cells and innervation on smooth muscle cell differentiation

Faggian, Luigi; Pampinella, Francesca; Roelofs, Marleen; Paulon, T.; Franch, Rafaella; Chiavegato, Angela; Sartore, Saverio

doi:10.1007/s004180050199

Cited by 32 publications

(18 citation statements)

References 39 publications

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“…Whether this decline is attributable to the total phenotypic transition of activated cells to fully differentiated smooth muscle cells or whether the activated cells revert back to a non-activated "non-muscle" cell type is a matter for speculation. Injury to the serosa or urinary outlet obstruction have been found to activate the proliferation of a population of subserosal mesenchymal cells (Roelofs et al 1995;Faggian et al 1998). It is noteworthy that the staining properties of these cells differ from the NM-MHC-B-positive cells in the present study in that they contain α-actin and NM-MHC-A.…”

Section: Discussioncontrasting

confidence: 64%

“…Mesenchymal cells have been detected in the subserosal layer by means of antibodies that recognize the 196-kDa NM-MHC-A and have been suggested to be able to transform into smooth muscle cells during hypertrophy and regeneration of the urinary bladder (Roelofs et al 1995;Buoro et al 1993;Faggian et al 1998). The 200-kDa NM-MHC-B is expressed in embryonic rabbit aorta smooth muscle in addition to SM1 (Kuro-o et al 1991).…”

Section: Introductionmentioning

confidence: 97%

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Increased expression of non-muscle myosin heavy chain-B in connective tissue cells of hypertrophic rat urinary bladder

Sjuve

Haase

Ekblad

et al. 2001

Cell and Tissue Research

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Expression of the non-muscle myosin heavy chain-B (NM-MHC-B, also denoted as the embryonic smooth muscle myosin heavy chain, SMemb) was examined in rat urinary bladder during growth in response to a partial urinary outflow obstruction. Following obstruction, the weight of the urinary bladder increased more than five-fold within 10 days. Immunohistochemistry with a polyclonal antiserum against the C-terminal sequence of NM-MHC-B revealed very few NM-MHC-B immunoreactive cells in the control urinary bladders. In hypertrophic bladders, the number of NM-MHC-B immunoreactive cells markedly increased. The majority of such cells were found in the interstitium surrounding smooth muscle bundles and also in the subserosal and submucosal layers. Western blot analysis showed that the NM-MHC-B expression was transient; the content of NM-MHC-B immunoreactive material had doubled 10 days after obstruction and then declined towards the control level after 6 weeks. Immunohistochemistry revealed co-localization of NM-MHC-B and vimentin within the same cells. NM-MHC-B did not co-localize with smooth muscle actin, suggesting that the source of NM-MHC-B is not a de-differentiated smooth muscle cell or myofibroblast but a non-muscle cell possibly reacting to tissue distension or stress. The NM-MHC-B-positive cells could have a role in the production of extracellular matrix and growth factors or be involved in modulation of spontaneous contractile activity.

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Section: Discussioncontrasting

confidence: 64%

Section: Introductionmentioning

confidence: 97%

Increased expression of non-muscle myosin heavy chain-B in connective tissue cells of hypertrophic rat urinary bladder

Sjuve

Haase

Ekblad

et al. 2001

Cell and Tissue Research

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“…If a localized necrosis is produced in the rabbit bladder wall, the healing process includes migration of ®broblasts into the injured smooth muscle bundles followed by differentiation into smooth muscle [Faggian et al, 1998]. …”

Section: Discussionmentioning

confidence: 99%

Regeneration of detrusor muscle after subtotal cystectomy in the rat: Effects on contractile proteins and bladder mechanics

Frederiksen

Sjuve

Arner

et al. 2001

Neurourology and Urodynamics

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The aim of the present study was to determine to what extent adult rats can produce new contracting bladder muscle and to see if such newly formed bladder tissue possesses characteristic mechanical properties or whether the ability to recover mechanically is so pronounced that the prehistory of the bladder is unimportant. Subtotal cystectomy was performed in adult female rats, leading to a pronounced decrease in total bladder weight. At 10 weeks, bladder weight had normalized. The histological appearance of such bladders was similar to that of the controls. Active and passive length-tension relations for the detrusor muscle were determined in controls and up to 10 weeks after surgery. Immediately after surgery active and passive forces showed a leftward shift and maximum active force decreased markedly. With time the length-tension curves shifted back to normal, but a decreased active force still remained at 10 weeks. Detrusor actin concentration and detrusor myosin/actin ratio were unaffected by the subtotal cystectomy. Intermediate filament protein/actin ratio showed a significant but transitory increase. We conclude that there is a remarkable recovery of detrusor muscle function after subtotal cystectomy, leading to a normalization of optimum length for active force and a net synthesis of contractile and cytoskeletal proteins. The ability to produce active force does, however, not fully recover.

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“…There are, however, some data that suggest that SM22 is also expressed in myofibroblasts from other experimental settings or in NM cell systems. In fact, serosal myofibroblasts from rabbit urinary bladder subjected to partial outflow obstruction 19 or transforming growth factor-␤1 infusion 41 contain SM22-expressing VAmyofibroblasts. SM22 is also expressed in vitro in rat embryo 42 and human senescent 43 fibroblasts, in the former as an actin gelling protein, transgelin.…”

Section: Phenotypic Changes In the Adventitiamentioning

confidence: 99%

“…The double immunofluorescence assays were performed using a monoclonal anti-SM-type ␣-actin (Sigma) directly coupled with fluorescein isothiocyanate and the anti-BrdU antibody indirectly revealed with the anti-mouse IgG conjugated with rhodamine isothiocyanate. 32 BrdU-incorporating nuclei in normal and injured vascular tissue from pulse and end labeling were detected using a specific anti-BrdU antibody (Dako) according to the procedure reported by Faggian et al 19 Negative and positive BrdU-incorporating tissues (myocardium and small intestine, respectively) from the same animals used for BrdU labeling of injured vessels were used as controls.…”

Section: Immunocytochemistrymentioning

confidence: 99%

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

Faggin

Puato

Zardo

et al. 1999

ATVB

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Abstract-During the "response-to-injury" process after a mechanical insult to the porcine coronary arteries, the adventitial cells acquire the structural characteristics of myofibroblasts before being incorporated into smooth muscle (SM) layer.We assessed whether the SM-specific SM22 protein can be used as a tracer of adventitial cell-myofibroblast differentiation in the mild balloon injury of rabbit carotid artery. To achieve this goal, we used 2 monoclonal anti-SM22 antibodies (E-11 and 1-B8) and a molecular probe for the SM22␣ mRNA isoform in immunocytochemical and in situ hybridization experiments. The differentiation profile and the migratory and proliferative ability of activated adventitial cells were evaluated by a panel of antibodies to some SM and nonmuscle antigens and pulse-and end-labeling with bromo-deoxyuridine, respectively. In adventitial cells, SM22 antigenicity and SM22␣ mRNA were detectable at days 2 and 4 and, to a lesser extent, at days 7 and 21 after injury, particularly near the adventitia-media interface and mostly colocalizing with bromo-deoxyuridine-positive cells. The pulse-labeling experiments showed that the large majority of these cells penetrated the outermost layer of the tunica media without migrating to the subendothelial region. The phenotypic features of activated migrating and nonmigrating adventitial cells resembled those of vimentin-actin myofibroblast subtype and fetal-type SM cells. These findings indicate that a direct exposure of adventitia to the lumen is not required for phenotypic changes and proliferation/migration of these cells. After comparison of the SM22 expression in arterial vessels during early stages of development, we hypothesize that in the injured carotid artery the mural incorporation of adventitial cells and the spatiotemporal activation of SM22 expression are reminiscent of the vascular morphogenetic process and suggest the existence of a stem cell-like reservoir in adventitia. The early adventitial upregulation of SM22 expression in the injured vessel might be related to a multistep transition process in which nonmuscle cells are converted to myofibroblasts and, possibly, to SM cells. (Arterioscler Thromb Vasc Biol.

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Phenotypic changes in the regenerating rabbit bladder muscle. Role of interstitial cells and innervation on smooth muscle cell differentiation

Cited by 32 publications

References 39 publications

Increased expression of non-muscle myosin heavy chain-B in connective tissue cells of hypertrophic rat urinary bladder

Increased expression of non-muscle myosin heavy chain-B in connective tissue cells of hypertrophic rat urinary bladder

Regeneration of detrusor muscle after subtotal cystectomy in the rat: Effects on contractile proteins and bladder mechanics

Smooth Muscle-Specific SM22 Protein Is Expressed in the Adventitial Cells of Balloon-Injured Rabbit Carotid Artery

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