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Septic sera induces apoptosis and DNA fragmentation factor 40 activation in fibroblasts.

Abstract：

:Sepsis, the systemic response to infection, is the leading cause of death in the intensive care units worldwide. Septic patients can succumb through the development of early refractory hypotension or late multiple organ dysfunction. Misregulation of apoptosis during sepsis may contribute to cellular dysfunction and multiple organ dysfunction. Utilizing a tissue culture model which mimics the human disease, we demonstrate that the addition of sera derived from septic patients induces apoptosis in human fibroblast cells. Addition of septic sera to 2fTGH cells induced apoptosis by activating caspase 8, caspase 3 and DNA fragmentation factor 40 (DFF 40). Interestingly, the addition of septic sera to cells which lack STAT1 (U3A cells) did not activate DFF 40. U3A cells were also shown to be resistant to septic serum induced apoptosis. These data suggest that DFF 40 mediated apoptosis plays a significant role in mediating sepsis induced cellular dysfunction.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Brabant D,Michael P,Bleiblo F,Saleh M,Narain R,Tai TC,Ramana CV,Parrillo JE,Kumar A,Kumar A

doi

10.1016/j.bbrc.2011.07.080

subject

Has Abstract

pub_date

2011-08-26 00:00:00

pages

260-5

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(11)01315-5

journal_volume

412

pub_type

杂志文章

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