Urinary bladder organ hypertrophy is partially regulated by Akt1-mediated protein synthesis pathway

Qiao, Li‐Ya; Xia, Chunmei; Shen, Shanwei; Lee, Seong Ho; Ratz, Paul H.; Fraser, Matthew O.; Miner, Amy S.; Speich, John E.; Lysiak, Jeffrey J.; Steers, William D.

doi:10.1016/j.lfs.2018.03.041

Cited by 7 publications

(6 citation statements)

References 52 publications

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“…These changes in the protein composition of the extracellular matrix could disturb the water and polysaccharide content of ECM and possibly change the overall weight of the tissue. Finally, it is possible that the difference in weight might be also due to changes at post-transcriptional level which we cannot explain with only RNA-seq data [37]. Bearing in mind that overall bladder histology was not altered in GF mice, it is reasonable to hypothesize that different bladder components were proportionally reduced by a cumulative effect of complex regulatory network, controlled by microbiota, in which ECM genes may play a leading role.…”

Section: Discussionmentioning

confidence: 88%

Microbiota Alters Urinary Bladder Weight and Gene Expression

et al. 2020

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We studied the effect of microbiota on the transcriptome and weight of the urinary bladder by comparing germ-free (GF) and specific pathogen-free (SPF) housed mice. In total, 97 genes were differently expressed (fold change > ±2; false discovery rate (FDR) p-value < 0.01) between the groups, including genes regulating circadian rhythm (Per1, Per2 and Per3), extracellular matrix (Spo1, Spon2), and neuromuscular synaptic transmission (Slc18a3, Slc5a7, Chrnb4, Chrna3, Snap25). The highest increase in expression was observed for immunoglobulin genes (Igkv1-122, Igkv4-68) of unknown function, but surprisingly the absence of microbiota did not change the expression of the genes responsible for recognizing microbes and their products. We found that urinary bladder weight was approximately 25% lighter in GF mice (p = 0.09 for males, p = 0.005 for females) and in mice treated with broad spectrum of antibiotics (p = 0.0002). In conclusion, our data indicate that microbiota is an important determinant of urinary bladder physiology controlling its gene expression and size.

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Section: Discussionmentioning

confidence: 88%

Microbiota Alters Urinary Bladder Weight and Gene Expression

et al. 2020

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“…pBOO was caused by bladder wall inflammation, hypertrophy, and fibrosis (Siregar et al, 2022). Studies demonstrated that pBOO-induced bladder fibrosis was attributed to fibrosis, smooth muscle cell proliferation and hypertrophy, and urothelium proliferation (Qiao et al, 2018). In female pBOO rats, the bladder smooth muscle progresses in hematoxylin and eosin staining and is confirmed by increased bladder mass and thickness increase (Metcalfe et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

YAP-mediated mechanotransduction in urinary bladder remodeling: Based on RNA-seq and CUT&Tag

Xiang

Jian

2023

Front. Genet.

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Yes-associated protein (YAP) is an important transcriptional coactivator binding to transcriptional factors that engage in many downstream gene transcription. Partial bladder outlet obstruction (pBOO) causes a massive burden to patients and finally leads to bladder fibrosis. Several cell types engage in the pBOO pathological process, including urothelial cells, smooth muscle cells, and fibroblasts. To clarify the function of YAP in bladder fibrosis, we performed the RNA-seq and CUT&Tag of the bladder smooth muscle cell to analyze the YAP ablation of human bladder smooth muscle cells (hBdSMCs) and immunoprecipitation of YAP. 141 differentially expressed genes (DEGs) were identified through RNA-seq between YAP-knockdown and nature control. After matching with the results of CUT&Tag, 36 genes were regulated directly by YAP. Then we identified the hub genes in the DEGs, including CDCA5, CENPA, DTL, NCAPH, and NEIL3, that contribute to cell proliferation. Thus, our study provides a regulatory network of YAP in smooth muscle proliferation. The possible effects of YAP on hBdSMC might be a vital target for pBOO-associated bladder fibrosis.

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“…Reduced ECM in Ehlers-Danlos syndrome (which is associated with mutations impacting on fibrillar collagens and fragility of connective tissue 33 and in Marfan syndrome (associated with mutations in fibrillin-1) have been linked with an increased risk of urinary tract complications including vesico-ureteric reflux, diverticula 34 and rupture from overdistension 35 . Whilst conversely, increased fibrosis and collagen deposition during bladder outflow obstruction 36 , 37 has been associated with decreased compliance and reduced capacity to store urine.…”

Section: Discussionmentioning

confidence: 99%

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

Hindi

Williams

Zeef

et al. 2021

Sci Rep

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Diabetes mellitus (DM) is the leading cause of chronic kidney disease and diabetic nephropathy is widely studied. In contrast, the pathobiology of diabetic urinary bladder disease is less understood despite dysfunctional voiding being common in DM. We hypothesised that diabetic cystopathy has a characteristic molecular signature. We therefore studied bladders of hyperglycaemic and polyuric rats with streptozotocin (STZ)-induced DM. Sixteen weeks after induction of DM, as assessed by RNA arrays, wide-ranging changes of gene expression occurred in DM bladders over and above those induced in bladders of non-hyperglycaemic rats with sucrose-induced polyuria. The altered transcripts included those coding for extracellular matrix regulators and neural molecules. Changes in key genes deregulated in DM rat bladders were also detected in db/db mouse bladders. In DM rat bladders there was reduced birefringent collagen between detrusor muscle bundles, and atomic force microscopy showed a significant reduction in tissue stiffness; neither change was found in bladders of sucrose-treated rats. Thus, altered extracellular matrix with reduced tissue rigidity may contribute to voiding dysfunction in people with long-term DM. These results serve as an informative stepping stone towards understanding the complex pathobiology of diabetic cystopathy.

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Urinary bladder organ hypertrophy is partially regulated by Akt1-mediated protein synthesis pathway

Cited by 7 publications

References 52 publications

Microbiota Alters Urinary Bladder Weight and Gene Expression

Microbiota Alters Urinary Bladder Weight and Gene Expression

YAP-mediated mechanotransduction in urinary bladder remodeling: Based on RNA-seq and CUT&Tag

Experimental long-term diabetes mellitus alters the transcriptome and biomechanical properties of the rat urinary bladder

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