Disease relevance of DIBUTYRYL CYCLIC GMP

• The improvement in Chediak-Higashi syndrome polymorphonuclear leukocyte function by the addition of cholinergic agents and dibutyryl cGMP suggested disturbed intracellular cyclic nucleotide levels [1].

High impact information on DIBUTYRYL CYCLIC GMP

• Persistent phosphorylation over 30 min was obtained when exposure to AMPA was preceded by a 15 min perfusion of the slice with 8-bromo-cGMP, dibutyryl-cGMP, or calyculin A but not phorbol 12,13-diacetate [2].
• Dibutyryl cAMP, but not dibutyryl cGMP, had an analogous suppressive effect on in vitro [3H]dThd incorporation into DNA [3].
• SRIF mRNA levels and SRIF release were significantly (P < 0.025) increased (approximately 2-fold) by 1 microM dibutyryl cGMP, whereas sodium butyrate had no effect [4].
• Since dibutyryl cGMP itself was capable of increasing GFR, cGMP is the likely second messenger for ANF in vivo [5].
• Incubation of vascular smooth muscle cells with the membrane-permeable cGMP analogues, dibutyryl cGMP and 8-bromo-cGMP, failed to induce HO-1 gene expression [6].

Biological context of DIBUTYRYL CYCLIC GMP

• The membrane-permeable cGMP analog dibutyryl-cGMP attenuated the H(2)O(2)-induced decrease in cell viability, DNA ladder formation, nuclear condensation, reduction of the mitochondrial membrane potential, cytochrome c release from mitochondria, and caspase-3 activation in cultured astrocytes [7].
• In receptor binding assays, dibutyryl cGMP competed with 125I-labeled gastrin for binding to HCT 116 cells (IC50 = 1.8 mM) [8].
• Indeed, at high concentrations (> or =2 mM), dibutyryl-cGMP caused an inhibition of apoptosis [9].
• A protein kinase G (PKG) inhibitor KT5823 inhibited SNP-induced downregulation of GATA-4, while YC-1 (guanylyl cyclase activator) and dibutyryl cGMP (PKG activator) downregulated GATA-4 [10].
• Monobutyryl-cGMP and dibutyryl-cGMP had only an inhibitory effect on cAMP hydrolysis [11].

Anatomical context of DIBUTYRYL CYCLIC GMP

• Both 8-bromo-cGMP (Br-cGMP) and dibutyryl cGMP (db-cGMP) produced oscillatory [Ca2+]i increases in hepatocytes [12].
• Adding dibutyryl-cGMP or calcium ionophore to the endothelial cells could not mimic IL-1-induced penetration and finally IL-1 did not induce PKC translocation in endothelial cells [13].
• The A and B subunits of cholera toxin, PGF2 alpha, PGD2, and dibutyryl cGMP failed to induce mast cells [14].
• Marked morphological changes were observed in HCT 116 cells after treatment with 1 mM dibutyryl cGMP [8].
• The gastrin/CCK receptor antagonist dibutyryl cGMP inhibited the proliferation of two human colon carcinoma cell lines HCT 116 (EC50 = 1.3 mM) and CBS (EC50 = 2.5 mM) in a dose-dependent manner [8].

Associations of DIBUTYRYL CYCLIC GMP with other chemical compounds

• However, in contrast to the NO donors, dibutyryl cGMP did not increase glutathione excretion [15].
• Addition of dibutyryl-cGMP (db-cGMP) induced COX-2 expression in a manner similar to SNAP; this induction was blocked by a p38 inhibitor (SB202190), but not by a JNK inhibitor (SP600125) [16].
• Proglumide and dibutyryl cyclic GMP (dbGMP), two distinct competitive antagonists of CCK8, reversed the inhibitory actions of CCK8 [17].
• The effect of a cGMP analogue, dibutyryl cGMP (dbcGMP), on angiotensin II-(AII) and PMA-induced MLC phosphorylation (MLCP) was tested, in the presence of calyculin A (CA), an inhibitor of MLC-PP [18].
• Tail flick latency (TFL) was elevated following microinjection of both dibutyryl cyclic AMP (dbcAMP) was dibutyryl cyclic GMP (dbcGMP) at sites in the caudal reticular formation [19].

Gene context of DIBUTYRYL CYCLIC GMP

• PKA inhibitor (KT5720) abolished the dbcAMP-induced phosphorylation of PLD1, but dibutyryl cGMP (dbcGMP) failed to phosphorylate PLD1 [20].
• Increasing cellular cGMP with phosphodiesterase inhibitors, by stimulation of soluble guanylyl cyclase with YC-1 or with exogenous dibutyryl cGMP resulted in mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 3,6 (MEK3,6) activation and phosphorylation of p38 [21].
• Treatment with dibutyryl cGMP (DBcGMP) dose-dependently increased the phosphorylation of both p44 and p42 isoforms of MAPK [22].
• Furthermore, dibutyryl-cGMP did not affect PGE(2)-accumulation. cANF, the specific ligand for the natriuretic peptide (NP) clearance-receptor (NPR-C), significantly inhibited PGE(2)-production [23].
• Whereas the abundance of POMC mRNA was found to be markedly suppressed following 4h of incubation with rANP(1-28) (0.01 to 1 microM), SNP (0.1 to 10 microM) and dibutyryl-cGMP (1 to 100 microM) in a dose related manner, only a modest reduction in the release and cell contents of beta EP-LI was found in some of these cultures [24].

Analytical, diagnostic and therapeutic context of DIBUTYRYL CYCLIC GMP

• The effect of dibutyryl cGMP (dbcGMP), a membrane permeant cGMP analogue, on cytosolic concentrations of Ca2+ ([Ca2+]i) was studied in cultured nodose ganglion neurons of the rabbit using fura-2AM and microfluorometry [25].
• Dibutyryl cGMP added to HT-2 cell cultures without IL-2 or in the presence of an optimal IL-2 concentration (60 U/ml) had no effect on proliferation [26].

References