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IGF-1 INDEPENDENT EFFECTS OF ESTRADIOL ON PROLIFERATION OF CULTURED BOVINE SATELLITE CELLS In BSC cultured in the presence of 10% fetal bovine serum, E2 treatment increases IGF-1 mRNA level ( Kamanga-Sollo et al., 2008a , b ). However, under culture conditions in which E2 treatment does not increase expression of IGF-1, IGF2, or IGF-1 receptor ( IGFR1 ), E2 treatment still stimulates proliferation in cultured BSC ( Kamanga-Sollo et al., 2008b ; Fig. 3 ). These data indicate that, in addition to stimulating BSC proliferation by increasing IGF-1 expression via interaction with the GPER-1 receptor, E2 may stimulate rate of proliferation through interaction with other receptors such as ESR1 ( Kamanga-Sollo et al., 2008a , b ). This possibility is further supported by the observation that ICI 182 780 (an ESR1 and ESR2 blocker) suppresses E2-stimulated BSC proliferation while actually stimulating IGF-1 mRNA transcription in cultured BSC ( Kamanga-Sollo et al., 2008b ). Additionally, E2-stimulated proliferation is completely abolished in BSC cultures in which ESR1 expression has been silenced by treatment with ESR1 specific small interfering RNA ( siRNA ; Kamanga-Sollo et al., 2013 ; Fig. 4 ). These data establish that ESR1 is required in order for E2 to stimulate proliferation of cultured BSC. In addition, the fact that treatment with ESR1 siRNA completely suppresses the ability of E2 to stimulate proliferation indicates that ESR2 (estrogen receptor-β) is not involved in E2-stimulated BSC proliferation.

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