PMID- 18563705 OWN - NLM STAT- MEDLINE DCOM- 20090807 LR - 20131121 IS - 1098-2795 (Electronic) IS - 1040-452X (Linking) VI - 76 IP - 3 DP - 2009 Mar TI - Regulatory changes of apoptotic factors in the bovine corpus luteum after induced luteolysis. PG - 220-30 LID - 10.1002/mrd.20946 [doi] AB - The corpus luteum (CL) offers the opportunity to study not only proliferative, but also regressive processes. During luteolysis of the CL a sudden death of luteal and endothelial cells seems to be involved (apoptosis). The aim of this study was to examen the mRNA expression of factors known to be involved in apoptotic processes: monocyte chemoattractant protein-1 (MCP-1), factors of the extrinsic and intrinsic apoptotic pathways, caspase3, -6, -7 and interferone gamma (IFNgamma). Luteolysis was induced by injection of 500 microg Cloprostenol during mid-luteal phase. The CLs were collected at 0.5, 2, 4, 12, 24, 48, and 64 hr after PGF2alpha-injection. Control CLs (Days 8-12) were collected at the slaugtherhouse. Real-time RT-PCR determined the mRNA expressions. Western blot analysis of poly(ADP-ribose) polymerase (PARP-1) and IFNgamma as well as protein measurement of tumor necrosis factor alpha (TNFalpha) by EIA were performed. The mRNA levels of MCP-1, IFNgamma and most factors of the extrinsic pathway were significantly increased between 0.5 and 2 hr. The factors of the intrinsic pathway were mostly later up-regulated at 24-48 hr after PGF2alpha. Caspase6 and 3 revealed a significant increase from 2 and 12 hr, respectively, whereas caspase7 was significantly up-regulated after 24 hr. The protein level of TNFalpha increased significantly to a maximum level at 12 hr. The Western blot revealed an increasing level of an 89 kDa fragment of PARP-1 from 12 to 24 hr, which is specific for apoptosis. We assume that the extrinsic pathway is more important for the onset of luteolysis, because of its earlier and higher increase during induced luteolysis. FAU - Kliem, H AU - Kliem H AD - Physiology Weihenstephan, Technical University Munich, Freising, Germany. FAU - Berisha, B AU - Berisha B FAU - Meyer, H H D AU - Meyer HH FAU - Schams, D AU - Schams D LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - United States TA - Mol Reprod Dev JT - Molecular reproduction and development JID - 8903333 RN - 0 (Antigens, CD) RN - 0 (Antigens, Differentiation, Myelomonocytic) RN - 0 (Apoptosis Regulatory Proteins) RN - 0 (CD163 antigen) RN - 0 (Chemokine CCL2) RN - 0 (Luteolytic Agents) RN - 0 (Proto-Oncogene Proteins c-bcl-2) RN - 0 (Receptors, CCR2) RN - 0 (Receptors, Cell Surface) RN - 0 (Tumor Necrosis Factor-alpha) RN - 0 (Tumor Suppressor Protein p53) RN - 4208238832 (Cloprostenol) RN - 4G7DS2Q64Y (Progesterone) RN - 82115-62-6 (Interferon-gamma) RN - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases) RN - EC 3.4.22.- (Caspases) SB - IM MH - Animals MH - Antigens, CD/genetics/metabolism MH - Antigens, Differentiation, Myelomonocytic/genetics/metabolism MH - Apoptosis/physiology MH - Apoptosis Regulatory Proteins/*genetics/*metabolism MH - Caspases/genetics/metabolism MH - Cattle MH - Chemokine CCL2/genetics/metabolism MH - Cloprostenol/pharmacology MH - Corpus Luteum/chemistry MH - Female MH - Gene Expression Regulation/drug effects/*physiology MH - Interferon-gamma/genetics/metabolism MH - Luteolysis/drug effects/*physiology MH - Luteolytic Agents/pharmacology MH - Poly(ADP-ribose) Polymerases/metabolism MH - Progesterone/blood MH - Proto-Oncogene Proteins c-bcl-2/genetics/metabolism MH - Receptors, CCR2/genetics/metabolism MH - Receptors, Cell Surface/genetics/metabolism MH - Tumor Necrosis Factor-alpha/genetics/metabolism MH - Tumor Suppressor Protein p53/genetics/metabolism EDAT- 2008/06/20 09:00 MHDA- 2009/08/08 09:00 CRDT- 2008/06/20 09:00 PHST- 2008/06/20 09:00 [pubmed] PHST- 2009/08/08 09:00 [medline] PHST- 2008/06/20 09:00 [entrez] AID - 10.1002/mrd.20946 [doi] PST - ppublish SO - Mol Reprod Dev. 2009 Mar;76(3):220-30. doi: 10.1002/mrd.20946.