No abstract

The possible role of second messenger systems in androgen-dependent smooth muscle proliferation was investigated. Focusing on the hormone-sensitive guinea pig seminal vesicle, we analyzed changes in protein kinase C (PKC) and cAMP-dependent type I and II protein kinases during the androgen-dependent smooth muscle proliferation of puberty, as well as in the transition to the nonproliferative state of the adult. The androgenic sensitivity of the cAMP-dependent type I and II protein kinases and the cAMP-dependent phosphorylations of soluble muscle proteins did not correlate with the qualitative change in the androgenic sensitivity of the prepubertal vs. adult animals. In contrast to the cAMP-dependent protein kinases, regulation of the soluble and particulate forms of PKC corresponded to the androgen-induced smooth muscle proliferation. That is, in the seminal vesicle muscle of prepubertal castrated animals, androgen treatment reduced both the soluble and particulate forms of PKC during the increase in smooth muscle DNA synthesis, and in adult seminal vesicle smooth muscle, which was resistant to androgen-induced proliferation, both forms of the enzyme were resistant to androgenic stimulation. It is concluded that PKC may be a component of an autocrine mitogenic mechanism involved in the coupling and uncoupling of androgen-induced smooth muscle proliferation.

The addition of retinoic acid to human promyelocytic leukemia cells in culture results in their differentiation to mature myeloid forms with acquisition of the differentiated phenotype, i.e., the ability to reduce nitroblue tetrazolium. A heavily pretreated patient with acute promyelocytic leukemia and residual malignant cells in his marrow after multiple courses of chemotherapy was given 134s-retinoic acid upon demonstration of both morphologic and functional differentiation of his leukemic cells by transretinoic acid in vitro. The patient achieved a complete remission and was maintained on 13-cis-retinoic acid for 1 year, when the patient relapsed. with a population of cells that were resistant to retinoic acid-induced differentiation.

No abstract

No abstract