Heated spermatozoa: effects on embryonic development and epigenetics  

Oleh:

Chao, Shi-Bin ; Guo, Lei ; Ou, Xiang-Hong ; Luo, Shi-Ming

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Human Reproduction vol. 27 no. 04 (Apr. 2012), page 1016-1024.
Topik: EARLY PREGNANCY; EMBRYOLOGY; Glycodelin-A; CD25; Eomesodermin; Bcl-2; Bax

Ketersediaan

Perpustakaan FK Nomor Panggil: H07.K.2012.01 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

BACKGROUND The progesterone-regulated glycoprotein glycodelin-A (GdA), secreted by the decidualized endometrium at high concentrations in primates, inhibits the maternal immune response against fetal antigens and thereby contributes to the tolerance of the semi-allogenic fetus during a normal pregnancy. Our earlier studies demonstrated the ability of GdA to induce an intrinsic apoptotic cascade in CD4+ T-lymphocytes and suppress the cytolytic effector function of CD8+ T-lymphocytes. In this report, we investigated further into the mechanism of action of GdA controlling perforin and granzyme B expression in CD8+ T-lymphocytes and the mechanism of action of GdA leading to lymphocyte death. METHODS Flow cytometry analysis was performed to check for the surface expression of interleukin-2 receptor a (IL-2Ra) and intracellular eomesodermin (Eomes) in activated T-lymphocytes, whereas quantitative RT–PCR analysis was used to find out their mRNA profile upon GdA treatment. Western analysis was carried out to confirm the protein level of Bax and Bcl-2. RESULTS GdA reduces the surface expression of the high-affinity IL-2R complex by down-regulating the synthesis of IL-2Ra (CD25). This disturbs the optimal IL-2 signalling and decreases the Eomes expression, which along with IL-2 directly regulates perforin and granzymes expression. Consequently, the CD8+ T-lymphocytes undergo growth arrest and are unable to mature into competent cytotoxic T-lymphocytes. In the CD4+ T-lymphocytes, growth factor IL-2 deprivation leads to proliferation inhibition, decreased Bcl-2/enhanced Bax expression, culminating in mitochondrial stress and cell death. CONCLUSIONS GdA spurs cell cycle arrest, loss of effector functions and apoptosis in different T-cell subsets by making T-lymphocytes unable to respond to IL-2.

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