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Mechanosensitive shivering of model tissues under controlled aspiration.

ABSTRACT: During embryonic development and wound healing, the mechanical signals transmitted from cells to their neighbors induce tissue rearrangement and directional movements. It has been observed that forces exerted between cells in a developing tissue under stress are not always monotonically varying, but they can be pulsatile. Here we investigate the response of model tissues to controlled external stresses. Spherical cellular aggregates are subjected to one-dimensional stretching forces using micropipette aspiration. At large enough pressures, the aggregate flows smoothly inside the pipette. However, in a narrow range of moderate aspiration pressures, the aggregate responds by pulsed contractions or "shivering." We explain the emergence of this shivering behavior by means of a simple analytical model where the uniaxially stretched cells are represented by a string of Kelvin-Voigt elements. Beyond a deformation threshold, cells contract and pull on neighboring cells after a time delay for cell response. Such an active behavior has previously been found to cause tissue pulsation during dorsal closure of Drosophila embryo.

SUBMITTER: Guevorkian K

PROVIDER: S-EPMC3158194 | biostudies-literature | 2011 Aug

REPOSITORIES: biostudies-literature

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Mechanosensitive shivering of model tissues under controlled aspiration.

Guevorkian Karine K Gonzalez-Rodriguez David D Carlier Camille C Dufour Sylvie S Brochard-Wyart Françoise F

Proceedings of the National Academy of Sciences of the United States of America 20110715 33

During embryonic development and wound healing, the mechanical signals transmitted from cells to their neighbors induce tissue rearrangement and directional movements. It has been observed that forces exerted between cells in a developing tissue under stress are not always monotonically varying, but they can be pulsatile. Here we investigate the response of model tissues to controlled external stresses. Spherical cellular aggregates are subjected to one-dimensional stretching forces using microp ...[more]

PMID: 21771735

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Project description:BackgroundDexmedetomidine, a highly selective ?2-adrenoceptor agonist, has been investigated for anti-shivering effects in some trials. This current meta-analysis was conducted to evaluate the effectiveness of dexmedetomidine as a neuraxial adjuvant in preventing perioperative shivering.MethodsThis systematic review and meta-analysis was registered in PROSPERO [www.crd.york.ac.uk/PROSPERO] with the unique identification number CRD42017055991. The electronic databases PubMed, Embase, Cochrane Central Register of Controlled Trials (CENTRAL) were searched to select high-quality randomized controlled trials (RCTs) that evaluated the anti-shivering efficacy for neuraxial application dexmedetomidine as local anesthetic adjuvant. Effects were summarized using pooled risk ratios (RRs), weighed mean differences (MDs), or standardized mean differences (SMDs) and corresponding 95% confidence intervals (Cls) with random effect model. Heterogeneity assessment, sensitivity analysis, and publication bias were performed. The primary outcome was perioperative shivering.ResultsA total of 1760 patients from 24 studies were included in this meta-analysis. Compared with the placebo, dexmedetomidine reduced the incidence of perioperative shivering (RR: 0.34; 95% Cl: 0.21 to 0.55; P < 0.00001), with a maximum effective dose of 5?g via subarachnoid space injection (RR: 0.55; 95% CI: 0.32 to 0.92; P = 0.02), especially in cesarean section (RR: 0.20; 95% CI: 0.09 to 0.45; P = 0.0001). Dexmedetomidine also could improve the characteristics of the block, with an increase only in the incidence of bradycardia (RR: 2.11; 95% CI: 1.23 to 3.60; P = 0.006). No significant difference could be found compared dexmedetomidine with other adjuvants, except morphine.ConclusionsThis meta-analysis shows that dexmedetomidine as a neuraxial adjuvant had statistically significant efficacy on prevention of perioperative shivering. Moreover, dexmedetomidine could improve the characteristics of the block. However, the potential induction of bradycardia should be taken seriously.

Project description:Objective: The vulnerability of atherosclerotic plaques is among the leading cause of ischemic stroke. High wall shear stress (WSS) promotes the instability of atherosclerotic plaques by directly imparting mechanical stimuli, but the specific mechanisms remain unclear. We speculate that modulation of mechanosensitive genes may play a vital role in accelerating the development of plaques. The purpose of this study was to find mechanosensitive genes in vascular endothelial cells (ECs) through combining microarray data with bioinformatics technology and further explore the underlying dynamics-related mechanisms that cause the progression and destabilization of atherosclerotic plaques. Methods: Microarray data sets for human vascular ECs under high and normal WSS were retrieved from the Gene Expression Omnibus (GEO) database. Differentially expressed genes (DEGs) were identified through the R language. The performance of enrichment analysis and protein-protein interaction (PPI) network presented the biological function and signaling pathways of the DEGs. Hub genes were identified based on the PPI network and validated by GEO data sets. Predicted transcription factor (TF) genes and miRNAs interaction with potential mechanosensitive genes were identified by NetworkAnalyst. Results: A total of 260 DEGs, 121 upregulated and 139 downregulated genes, were screened between high and normal WSS from GSE23289. A total of 10 hub genes and four cluster modules were filtered out based on the PPI network. The enrichment analysis showed that the biological functions of the hub genes were mainly involved in responses to unfolded protein and topologically incorrect protein, and t to endoplasmic reticulum stress. The significant pathways associated with the hub genes were those of protein processing in the endoplasmic reticulum, antigen processing, and presentation. Three out of the 10 hub genes, namely, activated transcription factor 3 (ATF3), heat shock protein family A (Hsp70) member 6 (HSPA6), and dual specificity phosphatase 1 (DUSP1, also known as CL100, HVH1, MKP-1, PTPN10), were verified in GSE13712. The expression of DUSP1 was higher in the senescent cell under high WSS than that of the young cell. The TF-miRNA-mechanosensitive gene coregulatory network was constructed. Conclusion: In this work, we identified three hub genes, ATF3, HSPA6, and DUSP1, as the potential mechanosensitive genes in the human blood vessels. DUSP1 was confirmed to be associated with the senescence of vascular ECs. Therefore, these three mechanosensitive genes may have emerged as potential novel targets for the prediction and prevention of ischemic stroke. Furthermore, the TF-miRNA-mechanosensitive genes coregulatory network reveals an underlying regulatory mechanism and the pathways to control disease progression.

Project description:Knee osteoarthritis (OA) results, at least in part, from overloading and inflammation leading to cartilage degradation. Prostaglandin E2 (PGE2) is one of the main catabolic factors involved in OA. Its synthesis is the result of cyclooxygenase (COX) and prostaglandin E synthase (PGES) activities whereas NAD+-dependent 15 hydroxy prostaglandin dehydrogenase (15-PGDH) is the key enzyme implicated in the catabolism of PGE2. For both COX and PGES, three isoforms have been described: in cartilage, COX-1 and cytosolic PGES are constitutively expressed whereas COX-2 and microsomal PGES type 1 (mPGES-1) are inducible in an inflammatory context. COX-3 (a variant of COX-1) and mPGES-2 have been recently cloned but little is known about their expression and regulation in cartilage, as is also the case for 15-PGDH. We investigated the regulation of the genes encoding COX and PGES isoforms during mechanical stress applied to cartilage explants. Mouse cartilage explants were subjected to compression (0.5 Hz, 1 MPa) for 2 to 24 hours. After determination of the amount of PGE2 released in the media (enzyme immunoassay), mRNA and proteins were extracted directly from the cartilage explants and analyzed by real-time RT-PCR and western blotting respectively. Mechanical compression of cartilage explants significantly increased PGE2 production in a time-dependent manner. This was not due to the synthesis of IL-1, since pretreatment with interleukin 1 receptor antagonist (IL1-Ra) did not alter the PGE2 synthesis. Interestingly, COX-2 and mPGES-1 mRNA expression significantly increased after 2 hours, in parallel with protein expression, whereas COX-3 and mPGES-2 mRNA expression was not modified. Moreover, we observed a delayed overexpression of 15-PGDH just before the decline of PGE2 synthesis after 18 hours, suggesting that PGE2 synthesis could be altered by the induction of 15-PGDH expression. We conclude that, along with COX-2, dynamic compression induces mPGES-1 mRNA and protein expression in cartilage explants. Thus, the mechanosensitive mPGES-1 enzyme represents a potential therapeutic target in osteoarthritis.

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Mechanosensitive shivering of model tissues under controlled aspiration.

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Mechanosensitive shivering of model tissues under controlled aspiration.

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