Mechanical Stretch Induces Platelet-activating Factor Receptor Gene Expression Through the NF-κB Transcription Factor

Chaqour, Brahim; Howard, Pamela S.; Richards, Charlotte F.; Macarak, Edward J.

doi:10.1006/jmcc.1999.0967

Cited by 45 publications

(42 citation statements)

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“…In cultured pulmonary artery smooth muscle cells, mechanical stretch induces platelet-derived activating factor (PAF) receptor gene expression, mediated by NF-B binding to the PAF receptor gene promoter. In these cells, protein kinase C activation is among the molecular features of NF-B activation and translocation into the nucleus in mechanically stretched cells (13). Mechanical stretch also plays an important role in TGF-␤1 gene upregulation and DNA binding of AP-1 through a stretch-induced signaling pathway in cultured human airway smooth muscle cells (31).…”

Section: Discussionmentioning

confidence: 99%

Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy

Boopathi

Gomes

Zderic

et al. 2014

American Journal of Physiology-Cell Physiology

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Boopathi E, Gomes C, Zderic SA, Malkowicz B, Chakrabarti R, Patel DP, Wein AJ, Chacko S. Mechanical stretch upregulates proteins involved in Ca 2ϩ sensitization in urinary bladder smooth muscle hypertrophy. Am J Physiol Cell Physiol 307: C542-C553, 2014. First published July 16, 2014; doi:10.1152/ajpcell.00033.2014.-Partial bladder outlet obstruction (pBOO)-induced remodeling of bladder detrusor smooth muscle (DSM) is associated with the modulation of cell signals regulating contraction. We analyzed the DSM from obstructed murine urinary bladders for the temporal regulation of RhoA GTPase and Rho-activated kinase (ROCK), which are linked to Ca 2ϩ sensitization. In addition, the effects of equibiaxial cell stretch, a condition thought to be associated with pBOO-induced bladder wall smooth muscle hypertrophy and voiding frequency, on the expression of RhoA, ROCK, and C-kinase-activated protein phosphatase I inhibitor (CPI-17) were investigated. DSM from 1-, 3-, 7-, and 14-day obstructed male mice bladders and benign prostatic hyperplasia (BPH)-induced obstructed human bladders revealed overexpression of RhoA and ROCK-␤ at the mRNA and protein levels compared with control. Primary human bladder myocytes seeded onto type I collagen-coated elastic silicone membranes were subjected to cyclic equibiaxial stretch, mimicking the cellular mechanical stretch in the bladder in vivo, and analyzed for the expression of RhoA, ROCK-␤, and CPI-17. Stretch caused a significant increase of RhoA, ROCK␤, and CPI-17 expression. The stretch-induced increase in CPI-17 expression occurs at the transcriptional level and is associated with CPI-17 promoter binding by GATA-6 and NF-B, the transcription factors responsible for CPI-17 gene transcription. Cell stretch caused by bladder overdistension in pBOO is the likely mechanism for initiating overexpression of the signaling proteins regulating DSM tone. partial bladder outlet obstruction; cell stretch; human bladder; benign prostatic hyperplasia; calcium sensitization DETRUSOR SMOOTH MUSCLE (DSM) hypertrophy is associated with alteration of the signaling pathways that initiate and maintain force in the bladder wall smooth muscle during partial bladder outlet obstruction (pBOO). These alterations have been observed in animal models and men with benign prostatic hyperplasia (BPH)-induced obstruction (7,9,14,19). In both animal models and humans, removal of the obstruction causes regression of smooth muscle hypertrophy, and the bladder function returns relatively to normal in most instances. However, in some cases, bladder function does not return to normal, and the reason for this is unclear. It is most likely due to the failure of altered signaling mechanisms to reverse back to normal, as seen in incomplete reversal of myosin isoform expression after 2-wk pBOO in rabbits (14).In general, activation of smooth muscle requires phosphorylation of the myosin regulatory light chain (MLC 20 ) by Ca 2ϩ / calmodulin-dependent myosin light chain kinase (MLCK) (2, 45). Under certain physiological cond...

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Section: Discussionmentioning

confidence: 99%

Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy

Boopathi

Gomes

Zderic

et al. 2014

American Journal of Physiology-Cell Physiology

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“…When the 5 -flanking regions of these three genes were compared, binding sites for NF-B, AP-1 and NF-IL6 were found, whereas a cAMP response element was present only in IL-6 and PBEF. The single NF-B response element in the 5 -flanking region of the PBEF gene, and the variant found in the third intron and NF-B-like elements present in introns 5, 8, 9 and 10, may be important for the regulation of this gene by mechanical distension (Nemeth et al 2000), as NF-B elements appear to be responsive to mechanical stimulation (Chaquour et al 1999). The latter authors showed that the expression of a transfected reporter gene bearing a 1·1 kb fragment of the promoter of the platelet-activating factor receptor gene (PAF-R) was enhanced in mechanically stretched pulmonary artery smooth muscle cells, indicating a direct effect on transcriptional activity.…”

Section: Discussionmentioning

confidence: 99%

“…The latter authors showed that the expression of a transfected reporter gene bearing a 1·1 kb fragment of the promoter of the platelet-activating factor receptor gene (PAF-R) was enhanced in mechanically stretched pulmonary artery smooth muscle cells, indicating a direct effect on transcriptional activity. When this was truncated, the promoterreporter construct lost this stretch inducibility (Chaquour et al 1999). This region in the PAF-R gene contained four copies of NF-B binding sites in close proximity to each other.…”

Section: Discussionmentioning

confidence: 99%

Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes

Ognjanovic

Bao²,

Yamamoto³

et al. 2001

Journal of Molecular Endocrinology

238

228

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Pre-B-cell colony enhancing factor (PBEF) was first isolated from an activated peripheral blood lymphocyte cDNA library and was found to be involved in the maturation of B-cell precursors. It was subsequently identified as one of the genes upregulated by distending the human fetal membranes in vitro. Here we report on the genomic organization of this gene, which is composed of 11 exons and 10 introns, spanning 34·7 kb of genomic DNA. Neither the gene nor the protein has any homology with other cytokines in any currently available database. The use of two promoters (proximal and distal) may result in differential, tissue specific expression of the PBEF transcripts. The 5 -flanking region lacks the classical sequence motif that would place it with the hematopoietic cytokines; however, it has several putative regulatory elements, suggesting that this gene may be chemically and mechanically responsive to inducers of transcription.The three PBEF mRNA transcripts were observed in both normal and infected human fetal membranes but were significantly upregulated (P<0·05) in severe infection. The PBEF protein was immunolocalized, in both normal and infected tissues, to both the normal fetal cells of the amnion and chorion and the maternal decidua of the membranes, and to the invading neutrophils. These stained strongly and were likely to contribute to the increased expression in infection. The amniotic epithelial cell line (WISH cells) has been used as a model to study PBEF gene modulation. Lipopolysaccharide, interleukin (IL)-1 , tumour necrosis factor (TNF) and IL-6 all significantly increased the expression of PBEF in 4 h of treatment. The addition of dexamethasone to IL-1 and TNF significantly reduced the response of PBEF to these cytokines. IL-8 treatment failed to alter PBEF gene expression. Thus PBEF is a cytokine expressed in the normal fetal membranes and upregulated when they are infected. It is likely to have a central role in the mechanism of infection-induced preterm birth.

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“…8 When the barriers that plasmid DNA must cross in order to successfully transfect a cell are examined, it becomes apparent that these same barriers are altered by exogenous mechanical forces, namely, alterations in the cytoskeleton and extracellular matrix, [9][10][11] activation of cell signaling pathways 12 and changes in transcription factor activation. 13,14 We concluded that because of the time course of cyclic stretch necessary to induce increased expression, as well as the ability for this enhancement to occur in cells transfected by either electroporation or liposomal transfection, the mechanisms responsible for the stretch-enhanced expression were at the level of either nuclear entry or cytoplasmic trafficking. In the present study, we have closely examined how cyclic stretch affects the cytoskeleton of our in vitro model.…”

Section: Introductionmentioning

confidence: 99%

Cyclic stretch-induced reorganization of the cytoskeleton and its role in enhanced gene transfer

et al. 2006

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Cyclic stretch is known to alter a number of cellular and subcellular processes, including those involved in nonviral gene delivery. We have previously shown that moderate equibiaxial cyclic stretch (10% change in basement membrane area, 0.5 Hz, 50% duty cycle) of human pulmonary A549 cells enhances gene transfer and expression of reporter plasmid DNA in vitro, and that this phenomena may be due to alterations in cytoplasmic trafficking. Although the path by which plasmid DNA travels through the cytoplasm toward the nucleus is not well understood, the cytoskeleton and the constituents of the cytoplasm are known to significantly hinder macromolecular diffusion. Using biochemical techniques and immunofluorescence microscopy, we show that both the microfilament and microtubule networks are significantly reorganized by equibiaxial cyclic stretch. Prevention of this reorganization through the use of cytoskeletal stabilizing compounds mitigates the stretchinduced increase in gene expression, however, depolymerization in the absence of stretch is not sufficient to increase gene expression. These results suggest that cytoskeletal reorganization plays an important role in stretch-induced gene transfer and expression. Gene Therapy (2006) 13, 725-731.

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Mechanical Stretch Induces Platelet-activating Factor Receptor Gene Expression Through the NF-κB Transcription Factor

Cited by 45 publications

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Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy

Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy

Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes

Cyclic stretch-induced reorganization of the cytoskeleton and its role in enhanced gene transfer

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Mechanical Stretch Induces Platelet-activating Factor Receptor Gene Expression Through the NF-κB Transcription Factor

Cited by 45 publications

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Mechanical stretch upregulates proteins involved in Ca2+ sensitization in urinary bladder smooth muscle hypertrophy

Mechanical stretch upregulates proteins involved in Ca2+ sensitization in urinary bladder smooth muscle hypertrophy

Genomic organization of the gene coding for human pre-B-cell colony enhancing factor and expression in human fetal membranes

Cyclic stretch-induced reorganization of the cytoskeleton and its role in enhanced gene transfer

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Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy

Mechanical stretch upregulates proteins involved in Ca²⁺ sensitization in urinary bladder smooth muscle hypertrophy