Cell communication induced by lysolecithin

Hax, W.M.A.; Venrooij, Ger E.P.M. van; Gon, J. J. Denier van der; Elbers, P. F.

doi:10.1007/bf01868220

Cited by 13 publications

(6 citation statements)

References 54 publications

(45 reference statements)

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“…In vitro capacitation of human spermatozoa leads to an accumulation of lysolecithin (47). Ultimately, increased membrane concentrations of lysolecithin create conditions for cell fusion (48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Localization of cholesteryl sulfate in human spermatozoa in support of a hypothesis for the mechanism of capacitation.

Langlais¹,

Zollinger²,

Plante³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

127

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Cholesteryl sulfate is a normal constituent of human spermatozoa. The in vitro uptake of tritiated cholesteryl sulfate resulted in the labeling of all spermatozoa as demonstrated by light-microscope radioautography. The binding of the sterol sulfate was localized mainly in the head and midpiece. Radioautography at the level of the electron microscope revealed that the sterol sulfate is localized on the plasma membrane, mostly in the region of the acrosome. Further proof for this localization was obtained by selective dissolution of the plasma membrane and acrosome of the spermatozoa with low concentrations of Triton X-100. This treatment resulted in the simultaneous removal of tritiated cholesteryl sulfate bound to the spermatozoa. A hypothesis is presented concerning the role of cholesteryl sulfate as a membrane stabilizer and enzyme inhibitor during the maturation of spermatozoa in the epididymis. According to this hypothesis, the cleavage ofthe sulfate moiety within the female reproductive tract triggers a cascade of events leading to sperm capacitation and fertilization. One of the challenges remaining in reproductive biology is the elucidation ofthe biochemical events involved in the maturation and capacitation of mammalian spermatozoa. A review of the literature (1)(2)(3)(4)(5) indicates that the following biochemical events occur during capacitation. Stabilizing factor(s), associated with the spermatozoal membrane during transit or storage within the epididymis inhibit the release ofacrosomal enzymes in the male tract, but the factor(s) must be removed during migration in the female tract to allow the contact of the acrosomal enzymes with the investments of the ovum in order to facilitate penetration. Removal ofthe stabilizing substance(s) is thought to be enzymecatalyzed and involves changes in membrane conformation and permeability, ultimately leading to the acrosome reaction.Evidence is accumulating in support of our contention that sterol sulfates play an important role in the biochemistry of sperm maturation and capacitation. Thus, we have reported that cholesteryl sulfate (CholSO4) is an important component of human spermatozoa and is avidly taken up by these cells during in vitro incubation (6, 7). In addition, during transit through the epididymis, hamster spermatozoa exhibit a severalfold increase in desmosteryl sulfate concentration from the caput to the cauda regions (8). The finding of sterol sulfotransferase activity in the hamster epididymis (9) demonstrates that the biosynthesis of sterol sulfates can occur in this tissue.That low concentrations of sterol sulfates can block in vitro capacitation by hamster cumulus cells (10) and also inhibit acrosin (11), the sperm acrosomal proteinase involved in the penetration of the zona pellucida of the ovum (12), provides evidence that sterol-sulfatase (sterol-sulfate sulfohydrolase, EC 3.1.6.2) could be involved in the mechanism of sperm capacitation and ovum penetration. Furthermore, sterol-sulfatase is present in the human female reproduct...

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Section: Discussionmentioning

confidence: 99%

Localization of cholesteryl sulfate in human spermatozoa in support of a hypothesis for the mechanism of capacitation.

Langlais¹,

Zollinger²,

Plante³

et al. 1981

Proc. Natl. Acad. Sci. U.S.A.

127

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“…In a previous paper (Hax, van Venrooij, Denier van der Gon & Elbers, 1973), it was demonstrated that lysophospholipids may act as an inductor for sites of low-resistance junctions between cells. As a consequence it was postulated that the concerted action of a phospholipase A and (an) acyltransferase (s) situated on the contact area of two adjacent cells, could regulate the permeability properties of the junctional membrane part by changing the lysophospholipid content of that particular part of the membrane.…”

Section: Mechanism Of Regulation Of Intercellular Communicationmentioning

confidence: 99%

Cell communication: A cyclic-AMP mediated phenomenon

1974

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“…In addition to fatty acids, the role of complex lipids in the process of communication between different cell types has also been investigated (Hax et al, 1973). Lipid transfer and interaction of platelet-activating factor between endothelial and smooth muscle cells in coculture has been reported by Spector (1987, 1989).…”

Section: Introductionmentioning

confidence: 99%

Effect of reduced levels of the LDL receptor of Ehrlich ascites tumor cells on cholesterol uptake and cell proliferation: A coculture study with baby hamster kidney cells

Haeffner

Wittmann

Kiesewetter

et al. 2007

Cell Biology International

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We have introduced a heterologous coculture model between Ehrlich ascites tumor (EAT) and baby hamster kidney cells (PtK2), and we have studied the influence of PtK2 cells and their newly synthesized cholesterol on uptake and tumor cell proliferation. PtK2 cells produce about five times more cholesterol as compared to EAT cells, and they support tumor cell growth in coculture experiments. This growth stimulation is reduced by 80% when EAT cells are cultured in PtK2 cell-derived medium in the presence of a monoclonal anti-low-density lipoprotein receptor (anti-LDL(r)) antibody. Freshly synthesized cholesterol by PtK2 cells is taken up by EAT cells in a time-dependent manner amounting to a threefold increase after 24 h. Alternatively, cholesterol transfer to EAT cells is decreased between 28% and 35%, when PtK2 cell cholesterol synthesis is inhibited in the presence of mevinolin, the specific inhibitor of the hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase. Furthermore, lower levels of EAT cell LDL receptor induced by antisense technology reduces cholesterol uptake and cell proliferation. These data demonstrate a metabolic interaction between normal and tumor cells mediated via the exchange of cholesterol, an important membrane constituent.

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Cell communication induced by lysolecithin

Cited by 13 publications

References 54 publications

Localization of cholesteryl sulfate in human spermatozoa in support of a hypothesis for the mechanism of capacitation.

Localization of cholesteryl sulfate in human spermatozoa in support of a hypothesis for the mechanism of capacitation.

Cell communication: A cyclic-AMP mediated phenomenon

Effect of reduced levels of the LDL receptor of Ehrlich ascites tumor cells on cholesterol uptake and cell proliferation: A coculture study with baby hamster kidney cells

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