Obstruction-induced alterations within the urinary bladder and their role in the pathophysiology of lower urinary tract symptomatology.

Komninos, Christos; Mitsogiannis, Iraklis

doi:10.5489/cuaj.1636

Cited by 24 publications

(23 citation statements)

References 70 publications

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“…Pathological tissue remodeling in bladders can be caused by BOO. These alterations include malfunction of urothelium, smooth muscle hypertrophy, and extracellular matrix (ECM) deposition that would result in LUTS, decreased bladder compliance, residual urine, and even dysfunction of the organ 4,5 . ECM accumulation is of great importance in the progression of BOO that can change the biomechanical properties of the bladder, leading to the transition from compensation to decompensation 6 …”

Section: Introductionmentioning

confidence: 99%

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Chen

Liao

Jin

et al. 2020

J of Cellular Biochemistry

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Extracellular matrix (ECM) accumulation plays a key role in the progression of bladder outlet obstruction (BOO). Muscarinic receptors have been widely reported to serve as pivotal regulators in lung tissue remodeling. However, the influence of them on human bladder smooth muscle cells (HBSMCs) and the underlying molecular mechanisms have not yet been evaluated. The purposes of the present study are to investigate the effect of muscarinic receptors on the synthesis of ECM in HBSMCs and the involvement of intracellular signal transducers. The results indicated that M1‐M5 muscarinic receptors were all encoded in HBSMCs. The expression rank order was M2 > M1 > M5 > M3 > M4. The gene and protein expression of collagen I (COL1), TIMP‐1, and TIMP‐2 was carbachol (CCH) concentration‐dependently enhanced. The synthesis of COL1 in the supernatant of cell culture medium was significantly elevated by exposure to CCH. The CCH‐induced protein expression of COL1, TIMP‐1, and TIMP‐2, however, was obviously reduced by the pretreatment of muscarinic receptor antagonists, atropine, and M3‐preferring antagonist (1,1‐dimethyl‐4‐diphenyl‐acetoxypiperidinium iodide [4‐DAMP]). Furthermore, ERK1/2 was activated by 100 µM CCH when compared with the control group and the pretreatment of ERK1/2 inhibitor significantly suppressed the synthesis of COL1 induced by 100 µM CCH. Besides, CCH‐induced phosphorylation of ERK1/2 was remarkably restrained by the pretreatment of 4‐DAMP. All in all, these findings demonstrated that M3 receptor can modulate extracellular matrix synthesis via the ERK1/2 signaling pathway, which may provide potential novel therapeutic targets for BOO.

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Section: Introductionmentioning

confidence: 99%

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Chen

Liao

Jin

et al. 2020

J of Cellular Biochemistry

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“…Patients with BPH have some degree of bladder outlet obstruction (BOO) and present to clinics with lower urinary tract symptoms (LUTS), such as urinary frequency, urgency, and nocturia . BOO could induce significant structural, functional, and biochemical changes in the bladder …”

Section: Introductionmentioning

confidence: 99%

Effects of varying degrees of partial bladder outlet obstruction on urinary bladder function of rats: A novel link to inflammation, oxidative stress and hypoxia

Kaya‐Sezginer

Yilmaz‐Oral

Lokman

et al. 2017

LUTS

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The results of the present study reveal the importance of oxidative stress-induced NF-κB signaling in bladder dysfunction with severe obstruction. Altered HIF signaling may contribute to the functional impairment after PBOO. Novel and evolving therapies targeting oxidative and/or inflammatory pathways may be a reasonable strategy for the management of lower urinary tract symptoms or benign prostatic hyperplasia.

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“…For example, in bladder outlet obstruction leading to obstructive uropathy, it is common to have a weak urine flow, straining, and decreased outflow of urine. 8 In contrast, patients with partial obstruction may have normal urine output or even polyuria. 9 Patients may also describe gross hematuria as their only symptom when presenting with obstruction.…”

Section: History Examination and Laboratory Findingsmentioning

confidence: 95%

Obstructive Uropathy

Girardi

Martin

2015

Hospital Medicine Clinics

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Obstruction-induced alterations within the urinary bladder and their role in the pathophysiology of lower urinary tract symptomatology.

Cited by 24 publications

References 70 publications

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Effects of varying degrees of partial bladder outlet obstruction on urinary bladder function of rats: A novel link to inflammation, oxidative stress and hypoxia

Obstructive Uropathy

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Obstruction-induced alterations within the urinary bladder and their role in the pathophysiology of lower urinary tract symptomatology.

Cited by 24 publications

References 70 publications

M3 receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

M3 receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

Effects of varying degrees of partial bladder outlet obstruction on urinary bladder function of rats: A novel link to inflammation, oxidative stress and hypoxia

Obstructive Uropathy

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M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells

M₃ receptor modulates extracellular matrix synthesis via ERK1/2 signaling pathway in human bladder smooth muscle cells