Detail of "80146-85-6"

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Modulation and transglutaminase activity in mononuclear phagocytes and macrophage-like tumor cell lines by differentiation agents

Modulation and transglutaminase activity in mononuclear phagocytes and macrophage-like tumor cell lines by differentiation agents. Goldman, Rachel (Dep. Membrane Res., Weizmann Inst. Sci., Rehovot 76100, Israel). Exp. Cell Res., 168(1), 31-43 (English) 1987. CODEN: ECREAL. ISSN: 0014-4827. DOCUMENT TYPE: Journal CA Section: 2 (Mammalian Hormones) The effect of glucocorticosteroids, retinoids, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) [32222-06-3] and the tumor promoter phorbol myristate acetate (TPA) [16561-29-8] on the expression of transglutaminase [80146-85-6] activity in in vitro differentiating bone marrow-derived mononuclear phagocytes (BMDMP) of mouse and rat and in mouse and human myeloid leukemia cell lines was assessed. Dexamethasone [50-02-2] induced an increase of about 100% in transglutaminase activity in mouse and rat BMDMP. The effect was time and dose dependent, and specific for steroids with glucocorticoid activity. Retinoic acid (RA) [302-79-4] suppressed transglutaminase activity in mouse BMDMP (~50%), but enhanced it in rat BMDMP (100-200%). Other retinoids were less effective. 1,25(OH)2D3 had little effect on transglutaminase expression in mouse BMDMP and suppressed it in rat BMDMP (~60%). TPA exerted a suppressive effect (~50%) on transglutaminase activity of both rat and mouse BMDMP. In murine (P388D1 and J774.2) and human (ML3, HL-60, KG-1, HEL, U937) myeloid leukemia cell lines, dexamethasone enhanced transglutaminase activity to a varying degree (100-1000%), RA suppressed it in P388D1 cells (~70%) and enhanced it in the other cell lines (100-1500%), 1,25(OH)2D3 induced a rather small augmentation of enzyme expression, and TPA suppressed enzyme expression (70-100%). The species-specific differences previously obsd. for the effect of RA, dexamethasone, and 1,25(OH)2D3 on the formation of BMDMP from mouse and rat bone marrow progenitor cells apparently extend also to effects on expression of transglutaminase activity. From a mechanistic point of view, it is of interest that dexamethasone uniformly enhanced transglutaminase activity, whereas TPA suppressed it. RA and 1,25(OH)2D3 induced either suppression or enhancement in the various cell types, with no correlation between the direction of the effect of the two agents. Thus, modulation of transglutaminase activity by the four agents may occur via disparate mechanisms.

Retinoic acid-induced expression of tissue transglutaminase in mouse peritoneal macrophages

Retinoic acid-induced expression of tissue transglutaminase in mouse peritoneal macrophages. Moore, William T., Jr.; Murtaugh, Michael P.; Davies, Peter J. A. (Med. Sch., Univ. Texas, Houston, TX 77025, USA). J. Biol. Chem., 259(20), 12794-802 (English) 1984. CODEN: JBCHA3. ISSN: 0021-9258. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Section cross-reference(s): 13 The culture of peritoneal macrophages in serum-contg. media induces a dramatic increase in the expression of the enzyme tissue transglutaminase [80146-85-6]. The transglutaminase-inducing activity of serum is abolished by extn. of lipids and fully restored by readdn. of physiol. concns. (1-100 nm) of all trans-retinoic acid [302-79-4]. Induction of the enzyme is detectable within a 90-min exposure of macrophages to retinoic acid and is completely blocked by actinomycin D, suggesting that the retinoid rapidly increases the rate of transglutaminase gene expression. Delipidized serum is required to elicit the transglutaminase-inducing activity of retinoic acid and this effect is decreased if the serum is depleted of the serum retinol-binding protein. These studies suggest that retinoic acid and serum retinol-binding protein can directly regulate macrophage gene expression and specifically induce the synthesis of tissue transglutaminase.