TY - JOUR
T1 - Modulation of the response to estradiol-17β of rat vascular tissues by a non calcemic vitamin D analog
AU - Somjen, Dalia
AU - Katzburg, Sara
AU - Baz, Merav
AU - Stern, Naftali
AU - Posner, Gary H.
PY - 2004/5
Y1 - 2004/5
N2 - Estradiol-17β (E2) increases creatine kinase (CK) specific activity in aorta (Ao) and left ventricle of the heart (Lv) from rat females. In the present study, we analyzed the effects of pretreatment with the non calcemic analog of vitamin D, JK 1624 F2-2 (JKF) on the response to E 2 (either 0.5 or 5 μg/rat) of Ao and Lv from prepubertal female rats. JKF did not affect CK in either organ. However, pretreatment with JKF (0.1 ng/g body weight for 1 or 2 weeks) increased the CK response to E2 (0.5 μg/rat) by 50±10% in Ao and by 150±12% in Lv. The CK response to 5 μg/rat of E2 in intact female rats, was increased by 118±15% and 99±11% in the Ao and by 89±6% and 112±13% in the Lv, in animals treated daily with JKF for 1 or 2 weeks, respectively, before administration of E2. JKF also increased the response to 500 μg/rat raloxifene (Ral) by 47±8% in Ao and by 56±12% in Lv. Preliminary experiments showed that JKF treatment induced a ∼50% increase in estradiol receptor ERα in both organs. The results indicate that the vitamin D analog JKF upregulates the response and sensitivity of vascular tissues to E2, in association with increased expression of their ERα. These results should prompt examination of the possibility that the effects estrogen therapy in postmenopausal women can be augmented by vitamin D or its analogs.
AB - Estradiol-17β (E2) increases creatine kinase (CK) specific activity in aorta (Ao) and left ventricle of the heart (Lv) from rat females. In the present study, we analyzed the effects of pretreatment with the non calcemic analog of vitamin D, JK 1624 F2-2 (JKF) on the response to E 2 (either 0.5 or 5 μg/rat) of Ao and Lv from prepubertal female rats. JKF did not affect CK in either organ. However, pretreatment with JKF (0.1 ng/g body weight for 1 or 2 weeks) increased the CK response to E2 (0.5 μg/rat) by 50±10% in Ao and by 150±12% in Lv. The CK response to 5 μg/rat of E2 in intact female rats, was increased by 118±15% and 99±11% in the Ao and by 89±6% and 112±13% in the Lv, in animals treated daily with JKF for 1 or 2 weeks, respectively, before administration of E2. JKF also increased the response to 500 μg/rat raloxifene (Ral) by 47±8% in Ao and by 56±12% in Lv. Preliminary experiments showed that JKF treatment induced a ∼50% increase in estradiol receptor ERα in both organs. The results indicate that the vitamin D analog JKF upregulates the response and sensitivity of vascular tissues to E2, in association with increased expression of their ERα. These results should prompt examination of the possibility that the effects estrogen therapy in postmenopausal women can be augmented by vitamin D or its analogs.
KW - "Non hypercalcemic" vitamin D analogs
KW - Creatine kinase
KW - Estrogen
KW - Estrogen receptors α and β
UR - http://www.scopus.com/inward/record.url?scp=3042687356&partnerID=8YFLogxK
U2 - 10.1016/j.jsbmb.2004.03.022
DO - 10.1016/j.jsbmb.2004.03.022
M3 - מאמר
C2 - 15225797
AN - SCOPUS:3042687356
VL - 89-90
SP - 339
EP - 341
JO - Journal of Steroid Biochemistry and Molecular Biology
JF - Journal of Steroid Biochemistry and Molecular Biology
SN - 0960-0760
ER -
