Antiapoptotic factor

Rehman J, Traktuev D, Li J, Merfeld-Clauss S, Temm-Grove CJ, Bovenkerk JE, Pell CL, Johnstone BH, Considine RV, March KL. Secretion of angiogenic and antiapoptotic factors by human adipose stromal cells. Circulation 2004 109 1292-1298. 

Previous studies have reported that ERKs are characteristically associated with cell proliferation and protection from apoptosis (Bl, XI), while activation of JNK and p38 MAPK can promote apoptosis in many systems, including B lymphocytes (G5), cerebellar granule cells (K3), hematopoietic cells (K8), and neuronal cells (M3, XI). On the other hand, a recent report found that a pyridinyl imidazole, SB 202190, the specific inhibitor of p38 MAPK, by itself was sufficient to induce apoptosis in T lymphocyte Jurkat cells (N2). Moreover, Th-2-derived cytokine IL-5, the ERK activator and antiapoptotic factor for eosinophils, could also activate p38 MAPK in human eosinophils (BIO). We recently reported that cytokine IL-3, IL-5, and GM-CSF could prolong survival of human eosinophilic leukemic (EoL-1) cells through the transient activation of ERK (W15). On the other hand, activation of p38 MAPK in EoL-1 cells by the NSAID sodium salicylate (NaSal) could lead to apoptosis (W15). We also found that the suppression of ERK using ERK antisense phosphorothioate oligodeoxynucleotides could promote the apoptosis of peripheral blood eosinophils (W16). Moreover, we found that dexamethasone-induced apoptosis and activation of JNK and p38 MAPK activity in eosinophils are regulated by caspases (Z2). 

Chan JA, Krichevsky AM, Kosik KS. MicroRNA-21 is an antiapoptotic factor in human glioblastoma cells. Cancer Res 2005 65 6029-6033. 

Other putative effects of estrogens include preservation of autoregulatory function, an antioxidant effect, reduction of A(i production and neurotoxicity, reduced excitotoxicity, increased expression of antiapoptotic factor bcl-2, and activation of mitogen-activated protein kinase pathways. Also, there is overwhelming data indicating that estrogens enhance survival of neurons both in vitro and in vivo (Green and Simpkins, 2000). 

Rodriguez-Pereira, C., Suarez-Panaranda, J. M., Barros, F., Sobrido, M. J., Vasquez-Salvado, M., and Forteza, J. 2001. Analysis of 2 antiapoptotic factors in gliomas. Arch. Pathol. Lab. Med. 725 218-233. 

Nakagawa Y. (2004). Role of mitochondrial phospholipid hydroperoxide glutathione peroxidase (PHGPx) as an antiapoptotic factor. Biol. Pharm. Bull. 27 956-960. 

Fig. 6.6 Signaling pathways involved in AlVmediated apoptosis. The stimulation of the AT2 receptor leads to a slow elevation in cellular ceramide, a proapoptotic messenger. The more rapid AT2 response results in the activation of a protein phosphatase, which has been identified as either a protein phosphatase 2A or MAP kinase phosphatase 1. The activated phosphatase catalyzes the dephosphorylation and inactivation of ERK1/2. Because ERK1/2 maintains the viability of Bcl-2, the inactivation of ERK1/2 leads to the dephosphorylation and degradation of the antiapoptotic factor.

Further than providing nutrients, these hydrolysates may play an essential role in providing growth factors, antiapoptotic factors, or protein production stimulators in serum-free cultures (Ikonomou et al., 2003). 

In cultured tumor cells, resistance to taxanes is associated in some lines with increased expression of the mdr-1 gene and its product, the P-glycoprotein other resistant cells have P-tubulin mutations, and these latter cells may display heightened sensitivity to vinca alkaloids. Other cell lines display an increase in survivin, an antiapoptotic factor or aurora kinase, an enzyme that promotes completion of mitosis. The basis of clinical drug resistance is not known. Cell death occurs by apoptosis, but the effectiveness of paclitaxel against experimental tumors does not depend on an intact p53 gene product. 

Palmitic acid roles in NAFLD installation and development have been discussed. PA overloading is known to induce apoptotic cell death and a large number of molecular mechanisms have been implicated in this action nitric oxide (NO) synthesis, suppression of antiapoptotic factors such as Bcl-2 [163, 164] reactive oxygen species generation, endoplasmic reticulum stress [165], nuclear factor-kB activation [166],... 

Gerber, H.P., Dixit, V. and Ferrara, N. (1998a) Vascular endothelial growth factor induces expression of the antiapoptotic proteins Bcl-2 and Al in vascular endothelial cellsJ. Biol. Chem., 273, 13313-13316. 

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