Connective tissue and its growth factor CTGF distinguish the morphometric and molecular remodeling of the bladder in a model of neurogenic bladder

Altuntas, Cengiz Z.; Daneshgari, Firouz; İzgi, Kenan; Bicer, Fuat; Özer, Ahmet; Sakalar, Cagri; Grimberg, Kerry O.; Sayin, İsmail; Tuohy, Vincent K.

doi:10.1152/ajprenal.00273.2012

Cited by 39 publications

(49 citation statements)

References 30 publications

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“…In addition, CTGF was shown to . This study also found that CTGF can inhibit the degradation of human mesangial cellular matrix by increasing the expression of MMP-2, TIMP-1 and TIMP-3, and that anti-CTGF antibody can slow down the degradation of the matrix reduce resulting from the high sugar and TGF-β [16][17][18] . This indicates that CTGF can promote the occurrence and development of organ fibrosis through promoting ECM production and inhibiting ECM degradation.…”

Section: ■ Discussionsupporting

confidence: 52%

Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells

Jia

et al. 2017

Acta Cir. Bras.

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Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells The pulmonary artery was then extracted, the fibrous tunica externa dissected and the runica intima stripped. The myogenous tissues of the vascular middle layer of the artery were then cut into 1 mm³ tissue blocks, and seeded into the culture flasks with the density as 1cm -2 . After 2 h wall-adherent cultivation at 37°C and 5% CO 2 , M199 medium containing 10% fetal bovine serum (FBS) was added. A week later, cells had grown outwards from the tissue blocks; when the growth covered 70% of the area of the base of the vessel, the culture was passaged. The 3rd-generation cells were taken for slice culturing and an immunohistochemical method was performed to detect the expression of cellular α-SMA and to confirm the purity of the PASMCs.The PASMCs were then divided into five groups and cultured in M199 medium containing different additional components, and for 48 h and 72 h. The control group was cultivated in M199 medium with 10% FBS. Indeed, in this study, the control group is negative control. The CTGF group with 10% FBS + 50 ng/ml CTGF (PeproTech, USA), the CP group with 10% FBS + 50 ng/ml CTGF + 20 μmol/L PD98059 (Sigma, USA), the CL group with 10% FBS + 50 ng/ml CTGF + 10 μmol/L LY294002 (Sigma, USA) and the CPL group with 10% FBS + 50 ng/ml CTGF + 20 μmol/L PD98059 + 10 μmol/L LY294002. RT-PCRFor the RT-PCR, the cDNA sequences of rat collagen III, fibronectin and β-actin were downloaded from NCBI gene database, then the Primer Premier 5 software was used to design appropriate PCR primers. The primer sequences were in the Table 1.

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Section: ■ Discussionsupporting

confidence: 52%

Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells

Jia

et al. 2017

Acta Cir. Bras.

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“…S4). Genes associated with fibrosis such as Col1a1 ( collagen, type 1, alpha 1 ) and Ctgf1 ( connective tissue growth factor ) were also upregulated in chronic EAE, findings that are consistent with a previous report7. The muscle marker Des was stable, similar to what was observed for the mucosa markers (Supplementary Figs.…”

Section: Resultssupporting

confidence: 91%

mentioning

confidence: 60%

“…Similar to what is observed in humans with MS, rodents with EAE present CNS lesions with inflammation, demyelination, axonal loss and gliosis4, and display significant bladder dysfunction56789. In mice with EAE, significant increase in bladder size5, increase in micturition frequency, decrease in urine volume voided per micturition (UVVM), changes in morphology6 and expression of molecular markers of fibrosis among others7, have been observed with progression of the disease and increase in neurological deficit. In rats with EAE, cystometric analysis showed changes in detrusor activity, such as detrusor hyperreflexia (bladder overactivity) and detrusor areflexia89, which closely resemble urodynamic changes observed in MS patients10, and have been attributed to an imbalance between the inhibitory and excitatory stimulation within the spinal cord centers controlling the micturition reflex8.…”

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confidence: 60%

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Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model

Negoro

Lutz

Liou

et al. 2013

Sci Rep

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Bladder dysfunction is common in Multiple Sclerosis (MS) but little is known of its pathophysiology. We show that mice with experimental autoimmune encephalomyelitis (EAE), a MS model, have micturition dysfunction and altered expression of genes associated with bladder mechanosensory, transduction and signaling systems including pannexin 1 (Panx1) and Gja1 (encoding connexin43, referred to here as Cx43). EAE mice with Panx1 depletion (Panx1−/−) displayed similar neurological deficits but lesser micturition dysfunction compared to Panx1+/+ EAE. Cx43 and IL-1β upregulation in Panx1+/+ EAE bladder mucosa was not observed in Panx1−/− EAE. In urothelial cells, IL-1β stimulation increased Cx43 expression, dye-coupling, and p38 MAPK phosphorylation but not ERK1/2 phosphorylation. SB203580 (p38 MAPK inhibitor) prevented IL-1β-induced Cx43 upregulation. IL-1β also increased IL-1β, IL-1R-1, PANX1 and CASP1 expression. Mefloquine (Panx1 blocker) reduced these IL-1β responses. We propose that Panx1 signaling provides a positive feedback loop for inflammatory responses involved in bladder dysfunction in MS.

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“…Bladder “thick in its coats” (John Hunter, 1788) is accompanied with many diseases and disorders in human and animals suffering from bladder inflammation [13, 14], neurological impairment [15, 16], bladder outlet obstruction with a variety of origin [17–21], social stress [22], or as a natural effect of aging [18]. The urinary bladder is made of four layers.…”

Section: Introductionmentioning

confidence: 99%

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

2015

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The present study aims to systemically characterize the factors that are associated with urinary bladder organ enlargement in the spontaneously hypertensive rats (SHR). Material and Methods We compared the SHR to age-matched normotensive Wistar-Kyoto (WKY) control rats in the levels of bladder pro-inflammatory factors, collagen expression (type I), and detrusor smooth muscle growth. Key Findings Our results showed that enhanced inflammatory responses and fibrosis were key factors that were closely associated with bladder wall thickening in SHR. Specifically the mRNA levels of inflammatory factors interleukin (IL)-1α, IL-6 and TNFα were significantly higher in SHR than those in WKY. The SHR also had a higher number of mast cells in the suburothelium space. Type I collagen production was also significantly higher in SHR when compared to those in control rats. However, the smooth muscle content stayed the same in SHR and WKY rats. This was shown as that the ratio of α-smooth muscle actin (SMA) to the nuclear protein histone H3 showed no difference between these two rat strains. The mRNA and protein levels of proliferating cell nuclear antigen (PCNA) also showed no change in the urinary bladder of SHR and WKY. Further study showed that the phosphorylation level of Akt in the urinary bladder was not changed in SHR when compared to WKY. In contrast, the phosphorylation level of ERK1/2 was significantly higher in SHR bladder when compared to WKY. Significance These results suggest that inflammation and fibrosis are primary factors that may lead to urinary bladder hypertrophy in SHR.

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Connective tissue and its growth factor CTGF distinguish the morphometric and molecular remodeling of the bladder in a model of neurogenic bladder

Cited by 39 publications

References 30 publications

Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells

Roles of the ERK1/2 and PI3K/PKB signaling pathways in regulating the expression of extracellular matrix genes in rat pulmonary artery smooth muscle cells

Pannexin 1 involvement in bladder dysfunction in a multiple sclerosis model

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

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