Oestradiol Inhibition of Vascular Myointimal Proliferation Following Immune, Chemical and Mechanical Injury

2007 ◽  
pp. 139-149
Author(s):  
Marie L. Foegh ◽  
Yejun Zhao ◽  
Michel Farhat ◽  
Peter W. Ramwell
Keyword(s):  
Mechanical Injury

Autocrine Induction of DNA Synthesis by Mechanical Injury of Cultured Smooth Muscle Cells

1996 ◽  
Vol 16 (2) ◽  
pp. 187-193 ◽  
Author(s):  
Federico Calara ◽  
Sean Ameli ◽  
Anna Hultgårdh-Nilsson ◽  
Bojan Cercek ◽  
Joel Kupfer ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Dna Synthesis ◽  
Muscle Cells ◽  
Mechanical Injury ◽  
Cultured Smooth Muscle Cells

scholarly journals Caveolin-1 Regulates P2Y2 Receptor Signaling during Mechanical Injury in Human 1321N1 Astrocytoma

Biomolecules ◽  
2019 ◽  
Vol 9 (10) ◽  
pp. 622
Author(s):  
Magdiel Martínez ◽  
Namyr A. Martínez ◽  
Jorge D. Miranda ◽  
Héctor M. Maldonado ◽  
Walter I. Silva Ortiz
Keyword(s):  
Cell Viability ◽  
Mechanical Injury ◽  
P2y2 Receptor ◽  
Caspase 9 ◽  
Post Injury ◽  
Caveolin 1 ◽  
Receptor Coupling ◽  
Downstream Signaling ◽  
Astrocytoma Cells ◽  
1321N1 Astrocytoma

Caveolae-associated protein caveolin-1 (Cav-1) plays key roles in cellular processes such as mechanosensing, receptor coupling to signaling pathways, cell growth, apoptosis, and cancer. In 1321N1 astrocytoma cells Cav-1 interacts with the P2Y2 receptor (P2Y2R) to modulate its downstream signaling. P2Y2R and its signaling machinery also mediate pro-survival actions after mechanical injury. This study determines if Cav-1 knockdown (KD) affects P2Y2R signaling and its pro-survival actions in the 1321N1 astrocytoma cells mechanical injury model system. KD of Cav-1 decreased its expression in 1321N1 cells devoid of or expressing hHAP2Y2R by ~88% and ~85%, respectively. Cav-1 KD had no significant impact on P2Y2R expression. Post-injury densitometric analysis of pERK1/2 and Akt activities in Cav-1-positive 1321N1 cells (devoid of or expressing a hHAP2Y2R) revealed a P2Y2R-dependent temporal increase in both kinases. These temporal increases in pERK1/2 and pAkt were significantly decreased in Cav-1 KD 1321N1 (devoid of or expressing a hHAP2Y2R). Cav-1 KD led to an ~2.0-fold and ~2.4-fold decrease in the magnitude of the hHAP2Y2R-mediated pERK1/2 and pAkt kinases’ activity, respectively. These early-onset hHAP2Y2R-mediated signaling responses in Cav-1-expressing and Cav-1 KD 1321N1 correlated with changes in cell viability (via a resazurin-based method) and apoptosis (via caspase-9 expression). In Cav-1-positive 1321N1 cells, expression of hHAP2Y2R led to a significant increase in cell viability and decreased apoptotic (caspase-9) activity after mechanical injury. In contrast, hHAP2Y2R-elicited changes in viability and apoptotic (caspase-9) activity were decreased after mechanical injury in Cav-1 KD 1321N1 cells expressing hHAP2Y2R. These findings support the importance of Cav-1 in modulating P2Y2R signaling during mechanical injury and its protective actions in a human astrocytoma cell line, whilst shedding light on potential new venues for brain injury or trauma interventions.

Neuroprotection by propofol in acute mechanical injury: role of GABAergic inhibition

1996 ◽  
Vol 76 (4) ◽  
pp. 2412-2422 ◽  
Author(s):  
G. S. Hollrigel ◽  
K. Toth ◽  
I. Soltesz
Keyword(s):  
Cell Death ◽  
Gabaa Receptor ◽  
Granule Cells ◽  
Neuronal Survival ◽  
Brain Slices ◽  
Mechanical Injury ◽  
Protective Effects ◽  
General Anesthetic ◽  
Gabaa Receptor Antagonist

1. Whole cell patch-clamp and extracellular field recordings were obtained from granule cells of the dentate gyrus in 400-microns-thick brain slices of the adult rat to determine the actions of the intravenous general anesthetic 2,6-diisopropylphenol (propofol) on acute neuronal survival and preservation of synaptic integrity after amputation of dendrites (dendrotomy), and to determine the role of gamma-aminobutyric acid-A (GABAA)-receptor-mediated inhibition in the neuroprotective effects of propofol. The actions of propofol were compared with those exerted by another widely used intravenous general anesthetic, 5-ethyl-5-[1-methylbutyl]-2-thiobarbituric acid (thiopental). 2. Propofol (10 microM) increased the frequency (control: 5.9 +/- 0.9 Hz, mean +/- SE; propofol: 10.5 +/- 1.3 Hz) and the single-exponential decay time constant (tau D) (control: 4.5 +/- 0.2 ms; propofol: 15.3 +/- 1.5 ms) of miniature inhibitory postsynaptic currents (mIPSCs) recorded in control neurons. Thiopental (25 microM) also increased the tau D (14.3 +/- 0.9 ms) of mISPCs, but had no effect on mIPSC frequency. Both anesthetics potentiated mIPSCs at low concentrations (propofol: 5 microM; thiopental: 1 microM). Propofol and thiopental did not change the peak amplitude and rise times of mIPSCs. 3. Propofol (10 microM) was able to depress the excitability of control granule cells, as determined by the reduction in the amplitude of the orthodromic population spikes. This depression could be prevented by the GABAA receptor antagonist bicuculline (50 microM), indicating that propofol reduces excitability via GABAA receptor functions. 4. Propofol and thiopental were neuroprotectant (assessed by antidromic population responses 2-5 h after injury) if present before and during the amputation of the granule cell dendrites. The protective actions were dose dependent, and at high doses (propofol: 200 microM; thiopental: 400 microM) the anesthetics were as neuroprotective against dendrotomy-induced cell death as 2-amino 5-phosphovaleric acid (APV) and 6-cyano-7-nitroquinoxaline-2,3 dione (CNQX). The protective effects of the anesthetics were completely blocked with the GABAA receptor antagonists picrotoxin or bicuculline, and were mimicked by the GABAA receptor agonist muscimol (100 microM). 5. Propofol, in contrast to APV and CNQX, could not prevent the dendrotomy-induced Ca(2+)-dependent and long-lasting changes in mIPSC decay kinetics (appearance of a double-exponential, prolonged decay). 6. The protective effects of the anesthetics and those of APV and CNQX on neuronal survival were not significant when the drugs were applied after dendrotomy, indicating that dendrotomy carried out 150-200 microns from the soma without neuroprotective agents rapidly induces irreversible acute degeneration in most injured neurons. The failure to rescue cells from dendrotomy-induced injury did not result from a decreased sensitivity of the GABAA receptors to the anesthetics, because the potentiating effects of the anesthetics on mIPSCs from control and dendrotomized neurons were not different. 7. These data indicate that propofol potentiates synaptic inhibition pre- and postsynaptically, and, when present during dendrotomy, it can protect neurons from acute mechanical-injury induced cell death via potentiation of GABAA receptor functions. However, propofol fails to provide neuroprotection against dendrotomy-induced changes in synaptic physiology.

scholarly journals 61 ELIMINATION OF MITOCHONDRIA RELATED BIM/BID PROTEINS REDUCES CHONDROCYTE APOPTOSIS AFTER MECHANICAL INJURY

2011 ◽  
Vol 19 ◽  
pp. S33-S34
Author(s):  
E. Eisner ◽  
C.G. Davis ◽  
J.J. Shelton ◽  
R.S. Hotchkiss ◽  
C.C. Chen ◽  
...  
Keyword(s):  
Mechanical Injury ◽  
Chondrocyte Apoptosis
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