Phosphoinositide-specific phospholipase C in health and disease

Cocco, Lucio; Follo, Matilde Y.; Manzoli, Lucia; Suh, Pann‐Ghill

doi:10.1194/jlr.r057984

Cited by 139 publications

(117 citation statements)

References 92 publications

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“…Interestingly, PI-PLCb1 is involved in the MDS progression to acute myeloid leukemia and in the response to epigenetic drugs (20)(21)(22)(23)(24)(25)(26). Moreover, the nuclear splicing variant of PI-PLCb1 is a negative regulator of erythroid differentiation and is reduced in both erythropoietinresponder, low-risk patients with MDS and in normal hematopoietic progenitors induced to erythroid differentiation (7,27).…”

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confidence: 99%

Nuclear translocation of PKC‐ α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs)

et al. 2018

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PI-PLCβ1 is involved in cell proliferation, differentiation, and myelodysplastic syndrome (MDS) pathogenesis. Moreover, the increased activity of PI-PLCβ1 reduces the expression of PKC-α, which, in turn, delays the cell proliferation and is linked to erythropoiesis. Lenalidomide is currently used in low-risk patients with MDS and del(5q), where it can suppress the del(5q) clone and restore normal erythropoiesis. In this study, we analyzed the effect of lenalidomide on 16 patients with low-risk del(5q) MDS, as well as del(5q) and non-del(5q) hematopoietic cell lines, mainly focusing on erythropoiesis, cell cycle, and PI-PLCβ1/PKC-α signaling. Overall, 11 patients were evaluated clinically, and 10 (90%) had favorable responses; the remaining case had a stable disease. At a molecular level, both responder patients and del(5q) cells showed a specific induction of erythropoiesis, with a reduced γ/β-globin ratio, an increase in glycophorin A, and a nuclear translocation of PKC-α. Moreover, lenalidomide could induce a selective G/G arrest of the cell cycle in del(5q) cells, slowing down the rate proliferation in those cells. Altogether, our results could not only better explain the role of PI-PLCβ1/PKC-α signaling in erythropoiesis but also lead to a better comprehension of the lenalidomide effect on del(5q) MDS and pave the way to innovative, targeted therapies.-Poli, A., Ratti, S., Finelli, C., Mongiorgi, S., Clissa, C., Lonetti, A., Cappellini, A., Catozzi, A., Barraco, M., Suh, P.-G., Manzoli, L., McCubrey, J. A., Cocco, L., Follo, M. Y. Nuclear translocation of PKC-α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs).

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Nuclear translocation of PKC‐ α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs)

et al. 2018

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“…The CaS-R on the parathyroid cell transduces hypercalcemia through Gq and/or Ga11, to activate phospholipase C, and thereby to raise inositol phosphates and to mobilize Ca++ from stores in the cytoplasm (Wettschureck N, Lee E, et al 2007; Conigrave AD, Ward DT 2013; Brown EM 2013; Hillenbrand M, Schori C, et al 2015; Cocco L, Follo MY, et al 2015; Nesbit MA, Hannan FM, et al 2013B ). Lowering of extracellular Ca++ or loss of function mutations of the CaS-R as in NSHPT stimulate secretion and hyperplasia in the parathyroid cells.…”

Section: Discussionmentioning

confidence: 99%

Hyperplasia in glands with hormone excess

Marx

2015

Endocrine-Related Cancer

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Five syndromes share predominantly hyperplastic glands with a primary excess of hormones: neonatal severe primary hyperparathyroidism, from homozygous mutated CASR, begins severely in utero; congenital non-autoimmune thyrotoxicosis, from mutated TSHR, varies from severe with fetal onset to mild with adult onset; familial male-limited precocious puberty, from mutated LHR, expresses testosterone oversecretion in young boys; hereditary ovarian hyperstimulation syndrome, from mutated FSHR, expresses symptomatic systemic vascular permeabilities during pregnancy; and familial hyperaldosteronism type IIIA, from mutated KCNJ5, presents in young children with hypertension and hypokalemia. The grouping of these five syndromes highlights predominant hyperplasia as a stable tissue endpoint and as their tissue stage for all of the hormone excess. Comparisons were made among this and two other groups of syndromes, forming a continuum of gland staging: predominant oversecretions express little or no hyperplasia; predominant hyperplasias express little or no neoplasia; and predominant neoplasias express nodules, adenomas, or cancers. Hyperplasias may progress (5 of 5) to neoplastic stages while predominant oversecretions rarely do (1 of 6; frequencies differ P!0.02). Hyperplasias do not show tumor multiplicity (0 of 5) unlike neoplasias that do (13 of 19; P!0.02). Hyperplasias express mutation of a plasma membrane-bound sensor (5 of 5), while neoplasias rarely do (3 of 14; P!0.002). In conclusion, the multiple distinguishing themes within the hyperplasias establish a robust pathophysiology. It has the shared and novel feature of mutant sensors in the plasma membrane, suggesting that these are major contributors to hyperplasia.

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“…The presence of these and other pollutants generates environmental signals whose perception is considered to occur at the cell membrane level (Sohlenkamp and Geiger, 2015). It is well known that some minor membrane PL, such as phosphoinositides (PPIns: phosphatidylinositol-4-phosphate [PtdIns-4-P], PtdIns-4,5-P) and phosphatidic acid (PtdOH), are associated with abiotic stress responses in eukaryote organisms (Armendariz et al, 2016;Cocco et al, 2015;Darwish et al, 2009;De Craene et al, 2017;Horváth et al, 2012;Ibañez et al, 2016;Martínez-Estévez et al, 2003;Ruelland et al, 2014;Xue et al, 2009). However, early signaling events involving signals mediated by lipids remain unexplored in bacteria.…”

Section: Introductionmentioning

confidence: 99%

Membrane Rigidity and Phosphatidic Acid (PtdOH) Signal: Two Important Events in Acinetobacter guillouiae SFC 500‐1A Exposed to Chromium(VI) and Phenol

Fernández

Paulucci

Margutti

et al. 2019

Lipids

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The remodeling of membrane lipids is a mechanism that allows microorganisms to survive in unfavorable environments such as industrial effluents, which often contain inorganic and organic pollutants, like chromium and phenol. In the present work, we evaluated the effect of Cr(VI) and phenol on the membrane of Acinetobacter guillouiae SFC 500‐1A, a bacterial strain isolated from tannery sediments where such pollutants can be found. The presence of lipid kinases and phospholipases and the changes in their activities under exposure to these pollutants were determined. Cr(VI) and Cr(VI) + phenol caused the membrane to become more rigid for up to 16 h after exposure. This could be due to an increase in cardiolipin (Ptd2Gro) and a decrease in phosphatidylethanolamine (PtdEtn), which are indicative of more order and rigidity in the membrane. Increased phospholipase A activity (PLA, EC 3.1.1.4) could be responsible for the decrease in PtdEtn levels. Moreover, our results indicate that Cr(VI) and Cr(VI) + phenol trigger the phosphatidic acid (PtdOH) signal. The finding of significantly increased phosphatidylinositol‐4‐phosphate (PtdIns‐4‐P) levels means this is likely achieved via PtdIns‐PLC/DGK. This report provides the first evidence that A. guillouiae SFC 500‐1A is able to sense Cr(VI) and phenol, transduce this signal through changes in the physical state of the membrane, and trigger lipid‐signaling events.

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Phosphoinositide-specific phospholipase C in health and disease

Cited by 139 publications

References 92 publications

Nuclear translocation of PKC‐ α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs)

Nuclear translocation of PKC‐ α is associated with cell cycle arrest and erythroid differentiation in myelodysplastic syndromes (MDSs)

Hyperplasia in glands with hormone excess

Membrane Rigidity and Phosphatidic Acid (PtdOH) Signal: Two Important Events in Acinetobacter guillouiae SFC 500‐1A Exposed to Chromium(VI) and Phenol

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