Role of Tumor Necrosis Factor α and Its Type I Receptor in Luteal Regression: Induction of Programmed Cell Death in Bovine Corpus Luteum-Derived Endothelial Cells

Friedman, Aharon; Weiss, Shay; Levy, Nizan; Meidan, Rina

doi:10.1095/biolreprod63.6.1905

Cited by 110 publications

(138 citation statements)

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“…These types of cells may have different regulatory mechanisms of cell death and the high expression of this protease suggests an important role of caspase-2 in the apoptotic death of these cells. Several studies demonstrated apoptosis of endothelial cells and suggested its activation through the tumor necrosis factor-a pathway (Friedman et al 2000, Pru et al 2003. Moreover, even though caspase-2 was the first mammalian apoptotic caspase identified (Kumar et al 1994, Wang et al 1994, little is known about its function.…”

Section: Discussionmentioning

confidence: 99%

“…It is known that initiator caspases are activated following direct association with death domain proteins. Interestingly, immune cells as well as cytokines were shown to play a role in regulating luteal function in rats, mice, cows, and women (Brannstrom & Friden 1997, Terranova & Rice 1997, Friedman et al 2000. Moreover, during luteolysis, macrophages are attracted and infiltrate in the CL, increasing the local production of cytokines (Brannstrom et al 1994).…”

Section: Discussionmentioning

confidence: 99%

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Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Peluffo¹,

Bussmann²,

Stouffer³

et al. 2006

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Apoptosis is associated with the regression of the corpus luteum (CL) in many species. Since caspases play a central role in apoptosis, we studied several initiators (-2, -8, and -9) and the main effector (-3) caspase in the CL during the estrous cycle of the rat. Two different populations of CL (old and new) were identified on ovaries at estrus and diestrus II (DII). Diminished (P!0.05) luteal progesterone content and P450scc levels suggested that functional luteolysis occurred between the new CL at DII and old CL at estrus, whereas the decline (P!0.05) in luteal weight indicated that structural regression was occurring between old CL at estrus to DII. Immunostaining for caspase-2 in luteal and endothelial cells appeared to increase as the luteal phase progressed, peaking at DII in the old CL. However, caspase-8 and -9 immunostaining showed little change with a slight increase at estrus in the old population. Notably, caspase-3 staining appeared to peak at DII in the new CL. Enzyme activity of caspase-9 increased (P!0.05) in the new CL at DII, followed by that of caspase-2 and -3 in old CL at estrus. Caspase-8 activity did not change at any stage. The number of apoptotic cells increased at DII in the old CL. These results suggest an important role for this protease family during early events of luteolysis in the rat estrous cycle. Reproduction (2006) 132 465-475

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Peluffo¹,

Bussmann²,

Stouffer³

et al. 2006

Reproduction

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“…Furthermore, TNF-a has an inhibitory effect on progesterone secretion in bovine luteal cells (37) and high TNF-a bioactivity has been observed in the PGF 2a -treated ovine corpus luteum (38). The TNF type I receptor is dominantly expressed in luteal endothelial cells (39). TNF receptor mRNA is induced in regressing luteal tissues and TNF may be a paracrine accelerator of luteal regression.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin F2α-Induced Functional Regression of the Corpus Luteum and Apoptosis in Rodents

et al. 2003

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Abstract. We investigated the relationship between prostaglandin (PG) F 2a -induced functional luteal regression and apoptosis in the rodent ovary. Administration of PGF 2a significantly decreased the serum levels of progesterone within 12 h after treatment in pseudopregnant mice. Apparent signals were detected in luteal tissues at 24 to 72 h by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick endo labeling (TUNEL) assay. PGF 2a significantly increased the levels of the cleavage nuclear poly (ADP-ribose) polymerase fragment and transforming growth factor-b (TGF-b) mRNA within 48 h. PGF 2a (10 m M) decreased progesterone secretion 6 to 72 h after its addition in luteinized ovarian cells, whereas C2-ceramide (25 m M) decreased progesterone levels by 44% 72 h after its addition. DNA fragmentation was not observed in the cultured cells treated with PGF 2a for 24 h, although cells incubated with C2-ceramide showed fragmentation. Treatment with PGF 2a for 1 h caused a distinct decrease in luteinizing hormone (LH)-induced cyclic AMP production. Thus, the inhibitory effect of PGF 2a on progesterone secretion may be caused by both the blockage of the functional LH receptor and the activation of apoptotic signaling.

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“…The different sensitivities of each cell type to TNF may be due to the difference in secretory products between LECs and LSCs. Progesterone secreted by LSCs has been shown to inhibit cell death in both LECs [17] and LSCs [29]. On the other hand, endothelin-1 (ET-1), a vasoactive peptide secreted by LECs, induces luteolysis in the bovine CL [30,31].…”

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confidence: 99%

Effects of Tumor Necrosis Factor .ALPHA. and Interferon .GAMMA. on the Viability and mRNA Expression of TNF Receptor Type I in Endothelial Cells from the Bovine Corpus Luteum

Hojo

Oda

Lee

et al. 2010

Journal of Reproduction and Development

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Abstract. The corpus luteum (CL) is mainly composed of luteal steroidogenic cells (LSCs) and luteal endothelial cells (LECs). Cell death of LSCs and LECs is essential for structural luteolysis. Therefore, it is important to understand the mechanisms regulating cell death in both types of luteal cells. We previously reported that a treatment combining tumor necrosis factor α (TNF) and interferon γ (IFNG) induced cell death in LSCs and that LECs express TNF receptor type I (TNFRI). To investigate the mechanism of cell death in LECs, in the present study we determined the effects of the same cytokines on cell viability and TNFRI mRNA expression in cultured LECs. To induce cell death in LECs, LECs were treated with TNF or IFNG (0, 0.05, 0.5, 1.0, 2.5 nM) and a combination of TNF (0.5 nM) and IFNG (0.5 nM) for 24 h. The viability of LECs was reduced by a single treatment with TNF or IFNG dose-dependently (P<0.05). Cell viability was further decreased by treatment with a combination of TNF and IFNG (P<0.05). Cells with DNA fragmentation (TUNEL-positive cells) were observed after the treatment with TNF and IFNG. Semi-quantitative RT-PCR analysis revealed that treatment with IFNG alone or in combination with TNF increased the expression of TNFRI mRNA compared with the control (P<0.05). In summary, TNF and IFNG increased cell death in cultured bovine LECs. The upregulation of TNFRI mRNA expression by IFNG suggests that TNF and IFNG synergistically affect the death of LECs resulting in acute luteolysis. Key words: Bovine, Cell death, Corpus luteum, Luteal endothelial cell, Luteolysis (J. Reprod. Dev. 56: [515][516][517][518][519] 2010) he corpus luteum (CL) is a transient organ that forms from the wall of a Graafian follicle following ovulation and secretes progesterone (P4) [1]. It reaches structural and functional maturity by the mid luteal phase and then begins to regress after Day 17 postovulation of a non-fertile cycle. In cows, luteal regression is characterized by a reduction in P4 production (functional luteolysis) and tissue degeneration by apoptosis (structural luteolysis) [2,3].Development of the bovine CL is associated with intensive angiogenesis [4], so that the mature CL becomes one of the most highly vascularized organs in the body [5][6][7], and vascular endothelial cells account for up to 50% of the total cells of the mid CL [8,9]. Recently, capillaries without smooth muscle and a few blood vessels with smooth muscle were found in the center of the mid bovine CL [10], and we reported that the capillaries disappeared, but not the large blood vessels during luteolysis [11]. Luteal endothelial cells (LECs) are the first cells to undergo programmed cell death (apoptosis) during luteal regression, resulting in the loss of capillaries [12,13].The number of leukocytes in the bovine CL (e.g., T lymphocytes, macrophages) increases at the time of luteolysis [14], and leukocytes are known to produce a variety of cytokines, including tumor necrosis factor α (TNF) and interferon γ (IFNG). A combination of IFNG and ...

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Role of Tumor Necrosis Factor α and Its Type I Receptor in Luteal Regression: Induction of Programmed Cell Death in Bovine Corpus Luteum-Derived Endothelial Cells

Cited by 110 publications

References 45 publications

Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Expression of caspase-2, -3, -8 and -9 proteins and enzyme activity in the corpus luteum of the rat at different stages during the natural estrous cycle

Prostaglandin F2α-Induced Functional Regression of the Corpus Luteum and Apoptosis in Rodents

Effects of Tumor Necrosis Factor .ALPHA. and Interferon .GAMMA. on the Viability and mRNA Expression of TNF Receptor Type I in Endothelial Cells from the Bovine Corpus Luteum

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