Morphometry of the obstructed detrusor: II. Principles of a comprehensive protocol

Meyer, Sabine; Elbadawi, Ahmad

doi:10.1002/nau.1930080210

Cited by 23 publications

(8 citation statements)

References 30 publications

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“…[19][20][21]. Several studies have also reported smooth muscle cell hyperplasia [20][21][22] and recent studies have…”

Section: Resultsmentioning

confidence: 99%

“…Many of these previous The main finding of this study is that systemic treatment studies relied on inappropriate techniques for quantifying with EGF induces smooth muscle cell hyperplasia in the smooth muscle volume and number (reviewed in [22]) urinary tract of mature Goettingen minipigs. This was and it is still debatable whether smooth muscle cell quantified in the ureters, but judging from the morhyperplasia occurs in the mature urinary tract.…”

Section: Discussionmentioning

confidence: 98%

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Chronic systemic treatment with epidermal growth factor induces smooth muscle cell hyperplasia and hypertrophy in the urinary tract of mature Goettingen minipigs

Vinter‐Jensen

Juhl²,

Dajani³

et al. 1997

British Journal of Urology

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Objective To determine the effect of systemic treatment 103 in the pigs treated with placebo and 55 (19-80) × 103 in those treated with EGF, and the median with epidermal growth factor (EGF) on the induction of growth in the urinary tract.(range) volume of the smooth muscle cells was 2.3 (2.2-2.4) × 103 and 4.0 (3.0-4.5) × 103 mm3 , Materials and methods Mature Goettingen minipigs were treated daily with vehicle (Tris-HCl; n=5) or EGF respectively. Conclusions There were two likely mechanisms contribu-(30 mg/kg) (n=6) for 4 weeks. The total number of smooth muscle cells was counted using an optical ting to smooth muscle cell hyperplasia, the division of fully differentiated smooth muscle cells and division of disector in a 20 mm thick cross-section of the ureter and the mean smooth muscle cell volume estimated.fibroblasts in the borderline between the submucosal layer and muscular coat, with ensuing differentiation Cell proliferation was detected by immunostaining for the marker Ki67.into smooth muscle cells. Treatment with EGF induces the growth of all wall layers in the urinary tract with Results The ureters of the animals treated with EGF were longer and thicker than those of the controls and the remarkable hyperplastic and hypertrophic changes of the smooth muscle cells in the muscular coat. median cross-sectional area of the ureter was 3.3-fold larger; the growth involved all wall layers. The median Keywords Epidermal growth factor, smooth muscle cells, hyperplasia, hypertrophy, pigs, urinary tract (range) number of smooth muscle cells in a 20 mm thick cross-section of the ureter was 11 (9-12) × suggested in vascular smooth muscle cells [6] and

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“…[19][20][21]. Several studies have also reported smooth muscle cell hyperplasia [20][21][22] and recent studies have…”

Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 98%

Chronic systemic treatment with epidermal growth factor induces smooth muscle cell hyperplasia and hypertrophy in the urinary tract of mature Goettingen minipigs

Vinter‐Jensen

Juhl²,

Dajani³

et al. 1997

British Journal of Urology

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show abstract

“…Another obstacle to further progress has been a failure to adopt the type of stereologically sound morphometric approaches used in fields such as neuroscience (55). Unlike other tissues (e.g., gut, bronchial airways), mammalian bladder smooth muscle cells lack a predictable organizational pattern (25,27,45). The obstructed detrusor also undergoes extensive structural plasticity (16,27,45) and any quantitative morphometry protocol must respect basic stereological principals to avoid possible biases (27,45,55).…”

Section: Mifmentioning

confidence: 99%

“…Unlike other tissues (e.g., gut, bronchial airways), mammalian bladder smooth muscle cells lack a predictable organizational pattern (25,27,45). The obstructed detrusor also undergoes extensive structural plasticity (16,27,45) and any quantitative morphometry protocol must respect basic stereological principals to avoid possible biases (27,45,55). The traditional collagen-to-muscle ratio provides only limited information since it does not establish the magnitude, or even the direction, of change involving either compartment.…”

Section: Mifmentioning

confidence: 99%

Null mutation in macrophage migration inhibitory factor prevents muscle cell loss and fibrosis in partial bladder outlet obstruction

Taylor¹,

Zhu²,

Irwin³

et al. 2006

American Journal of Physiology-Renal Physiology

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Idiopathic detrusor underactivity (DU) and detrusor decompensation which develops following partial bladder outlet obstruction (pBOO) are both associated with smooth muscle degeneration and fibrosis. Macrophage migration inhibitory factor (MIF), an important mediator of bladder inflammation, has been shown to promote fibroblast survival and muscle death in other tissues. We evaluated the hypothesis that MIF has similar actions in the bladder by studying detrusor responses to pBOO or sham surgery in anesthetized female mice rendered null for the mif gene (MIF KO) and in wild-type (WT) controls, all killed 3 wk after surgery. WT mice revealed intense MIF immunoreactivity in urothelial cells which decreased, without change in overall mif mRNA levels. Stereologically sound quantitative morphometric measurements were performed in the middetrusor region of each bladder. MIF KO bladders were normal in appearance, yet were 30-40% heavier, with increased middetrusor collagen and muscle, compared with WT controls. In WT mice, pBOO increased the collagen-to-muscle ratio 1.9-fold and middetrusor collagen 1.8-fold, while nucleated muscle counts were 22% lower. In MIF KO mice, by contrast, pBOO had no significant effect on any of these parameters. In primary bladder muscle cultures, treatment with rMIF protein increased TUNEL staining, raising the proportion of early and late apoptotic cells on flow cytometry. Our studies implicate MIF in the sequence of events leading to detrusor muscle loss and fibrosis in obstruction. They raise the possibility that strategies designed to antagonize MIF synthesis, release, or biological activity could prevent or delay DU and urinary retention.

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“…The limitations of morphometry in the detrusor center around the lack of a truly layered structural organization of its smooth muscle, the wide variations in its interstitial elements in different species, and the regional as well as species variability of its intrinsic innervation [Elbadawi and Meyer, 19891. Our recent morphologicimorphometric studies on the detrusor in a rabbit model of acutely induced, persistent, partial bladder outlet obstruction, with vesical overdistension, is perhaps the most comprehensive such study so far of any condition that can alter DC. These studies Elbadawi et al, 1989a,b;Meyer and Elbadawi, 1989;Meyer et al, 1989a,c]:…”

Section: Structural Basis Of Altered DCmentioning

confidence: 99%

Morphometry of the obstructed detrusor: II. Principles of a comprehensive protocol

Cited by 23 publications

References 30 publications

Chronic systemic treatment with epidermal growth factor induces smooth muscle cell hyperplasia and hypertrophy in the urinary tract of mature Goettingen minipigs

Chronic systemic treatment with epidermal growth factor induces smooth muscle cell hyperplasia and hypertrophy in the urinary tract of mature Goettingen minipigs

Null mutation in macrophage migration inhibitory factor prevents muscle cell loss and fibrosis in partial bladder outlet obstruction

Microstructural basis of detrusor contractility: The MIN approach to its understanding and study

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