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March 9, 1998Circulation ResearchOpen Access

Fas (CD95/Apo-1)–Mediated Damage to Ventricular Myocytes Induced by Cytotoxic T Lymphocytes From Perforin-Deficient Mice

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Key result

Perforin-deficient cytotoxic T lymphocytes and anti-Fas antibody induced electrophysiological dysfunction and calcium overload in murine ventricular myocytes via an IP3-mediated mechanism (P<0.05).

Population

Murine ventricular myocytes and peritoneal exudate cytotoxic T lymphocytes derived from perforin…

Comparison

Conjugation with P-/- PELs or treatment with… vs Nonconjugated myocytes

Design

Preclinical

Authors

BFBella FelzenRappaport Family Institute for Research in the Medical SciencesMSMark ShilkrutOlema Pharmaceuticals (United States)HLHadar LessTechnion – Israel Institute of Technology

Discussion

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Implication

Fas-mediated CTL injury may drive rejection and myocarditis; leaves open whether Fas targeting improves outcomes in patients.

Structured PICO

P
Population
Murine ventricular myocytes and peritoneal exudate cytotoxic T lymphocytes (PELs) derived from perforin gene-knockout (P-/-) mice
I
Intervention
Conjugation with P-/- PELs or treatment with apoptosis-inducing anti-Fas monoclonal antibody Jo2
C
Comparator
Nonconjugated myocytes
O
Outcome
Action potential characteristics, [Ca2+]i transients, and contractionssurrogate

Main Result

p-value: p=<.05

A Fas-based, perforin-independent mechanism of cytotoxic T lymphocyte action mediated by IP3 can cause ventricular myocyte dysfunction, providing insight into the immunopathology of heart transplant rejection, myocarditis, and dilated cardiomyopathy.

Cite This Study

Felzen et al. (1998) studied Myocarditis and cardiomyopathies. Perforin-deficient cytotoxic T lymphocytes (P-/- PELs) or anti-Fas antibody Jo2 vs. Nonconjugated myocytes was evaluated on Action potential characteristics and intracellular calcium transients (p=<.05). Perforin-deficient cytotoxic T lymphocytes and anti-Fas antibody induced electrophysiological dysfunction and calcium overload in murine ventricular myocytes via an IP3-mediated mechanism (P<0.05).

synapsesocial.com/papers/6a6c414e34b735385cb3ecdahttps://doi.org/10.1161/01.res.82.4.438
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Apoptosis in Myocytes in End-Stage Heart Failure1996 · 1,445 citations
  2. 2Anti-αβ T cell receptor antibody prevents the progression of experimental autoimmune myocarditis1994 · 38 citations
  3. 3Immune function in mice lacking the perforin gene.1994 · 463 citations
  4. 4Arrhythmogenic Action of Thrombin During Myocardial Reperfusion via Release of Inositol 1,4,5-Triphosphate1996 · 63 citations
  5. 5Cytosolic heparin inhibits muscarinic and α-adrenergic Ca2+ release in smooth muscle1989 · 342 citations