Basic fibroblast growth factor induces 3T3 fibroblasts to synthesize and secrete a cyclophilin-like protein and β2-microglobulin

Davis, Thomas R.; Tabatabai, Louisa B.; Bruns, Kerry A.; Hamilton, Richard T.; Nilsen-Hamilton, Marit

doi:10.1016/0167-4889(91)90077-b

Cited by 49 publications

(39 citation statements)

References 26 publications

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“…Results presented in this report demonstrate that HIV-1 infection can be inhibited in vitro by agents targeted to the interaction between virion-associated CyPA and putative CyPA-binding sites on CD4 existence of signal-transducing CyPA-binding sites is consistent with the published data reporting the presence of secreted CyP(s) in biological fluids (15,16) and culture medium supernatants (14,28), which possess functions usually attributed to cytokines and growth factors (14,16,29,30). A receptor for another member of the cyclophilin family, cyclophilin B (CyPB), which is highly homologous to CyPA, has been recently identified on CD4 ϩ T lymphocytes (31,32).…”

Section: Discussionsupporting

confidence: 79%

Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes

Sherry

Zybarth

Alfano

et al. 1998

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

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Cyclophilins are a family of proteins that bind cyclosporin A (CsA) and possess peptidyl-prolyl cis-trans isomerase activity. In addition, they are secreted by activated cells and act in a cytokine-like manner, presumably via signaling through a cell surface cyclophilin receptor. More recently, host-derived cyclophilin A (CyPA) has been shown to be incorporated into HIV-1 virions and its incorporation essential for viral infectivity. Here we present evidence supporting a role for viral-associated CyPA in the early events of HIV-1 infection. We report that HIV-1 infection of primary peripheral blood mononuclear cells can be inhibited by: (i) an excess of exogenously added CyPA; (ii) a CsA analogue unable to enter the cells; (iii) neutralizing antibodies to CyPA. Taken together with our observations that recombinant CyPAinduced mobilization of calcium in immortalized, as well as primary, CD4؉ T lymphocytes, and that incubation of T cells with iodinated CyPA, followed by chemical cross-linking, resulted in the formation of a high molecular mass complex on the cell surface, these results suggest that HIV-1-associated CyPA mediates an early event in viral infection via interaction with a cellular receptor. This interaction may present a target for anti-HIV therapies and vaccines.

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Section: Discussionsupporting

confidence: 79%

Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes

Sherry

Zybarth

Alfano

et al. 1998

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

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“…Interestingly, CHX in fact caused a further increase in lipocalin 2 expression. This finding has been previously reported (13) and could be due to CHX blocking the synthesis of a lipocalin 2 or Dex repressor.…”

Section: Discussionsupporting

confidence: 55%

Dexamethasone-induced expression of the glucocorticoid response gene lipocalin 2 in chondrocytes

Owen¹,

Roberts²,

Ahmed³

et al. 2008

American Journal of Physiology-Endocrinology and Metabolism

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Owen HC, Roberts SJ, Ahmed SF, Farquharson C. Dexamethasone-induced expression of the glucocorticoid response gene lipocalin 2 in chondrocytes. Am J Physiol Endocrinol Metab 294: E1023-E1034, 2008. First published April 1, 2008 doi:10.1152/ajpendo.00586.2007 are commonly used anti-inflammatory drugs, but long-term use can result in marked growth retardation in children due to their actions on growth plate chondrocytes. To gain an insight into the mechanisms involved in GC-induced growth retardation, we performed Affymetrix microarray analysis of the murine chondrogenic cell line ATDC5, incubated with 10 Ϫ6 M dexamethasone (Dex) for 24 h. Downregulated genes included secreted frizzled-related protein and IGF-I, and upregulated genes included serum/GC-regulated kinase, connective-tissue growth factor, and lipocalin 2. Lipocalin 2 expression increased 40-fold after 24-h Dex treatment. Expression increased further after 48-h (75-fold) and 96-h (84-fold) Dex treatment, and this response was Dex concentration dependent. Lipocalin 2 was immunolocalized to both proliferating and hypertrophic growth plate zones, and its expression was increased by Dex in primary chondrocytes at 6 h (3-fold, P Ͻ 0.05). The lipocalin 2 response was blocked by the GC-receptor antagonist RU-486 and was increased further by the protein synthesis blocker cycloheximide. Proliferation in lipocalin 2-overexpressing cells was less than in control cells (49%, P Ͻ 0.05), and overexpression caused an increase in collagen type X expression (4-fold, P Ͻ 0.05). The effects of lipocalin 2 overexpression on chondrocyte proliferation (64%, P Ͻ 0.05) and collagen type X expression (8-fold, P Ͻ 0.05) were further exacerbated with the addition of 10 Ϫ6

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“…The protein in the lipopolysaccharide-stimulated PU5·1·8 macrophage is suggested to function in the defense against infectious agents (Meheus et al 1993). The protein is also present in basic fibroblast growth factorstimulated 3T3 cells (Davis et al 1991). The study of Liu and Nilsen-Hamilton (1995) reveals that 24p3 protein is an acute phase protein of the liver.…”

Section: Introductionmentioning

confidence: 93%

Ovarian steroids regulate 24p3 expression in mouse uterus during the natural estrous cycle and the preimplantation period

Huang

Chu²,

Chen³

1999

Journal of Endocrinology

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We examined 24p3 expression in the mouse uterus at various stages of the natural estrous cycle and during the preimplantation period. The level of 24p3 mRNA appeared intensively in proestrus and estrus, then declined sharply from metestrus to diestrus. Consistent with this observation, 24p3 protein was abundant in proestrus, decreased from estrus to metestrus and declined to a very low level in diestrus. The uterine 24p3 expression closely overlapped with the estradiol (E 2 ) surge in proestrus and estrus but it was suppressed when progesterone (P 4 ) rose to a high level during the reproductive cycle. Neither the protein nor its message was detected in the uteri of immature mice or ovariectomized adult animals. While an injection of P 4 to these animals was unable to initiate uterine 24p3 expression, administration of estrogenic steroids to these animals markedly stimulated the gene expression. Treatment of these animals with E 2 together with P 4 , on the other hand, did not stimulate the gene expression. In pregnant animals (day 1 (D1)=day of vaginal plug), 24p3 mRNA remained at a high level on D1 and D2 but dropped to an almost undetectable level on D3 and D4. This was accompanied by a decrease in 24p3 protein from D1 to D2 and a decline in the protein to undetectable levels from D3 to D4. The staining patterns of both the immunohistochemical localization of 24p3 protein and in situ hybridization for the detection of 24p3 mRNA in the uterine sections showed that 24p3 expression took place mainly in the luminal and glandular epithelial cells of the endometrium. This together with our previous observation that 24p3 protein is found in uterine luminal fluid indicates that the protein is secreted primarily from these cells to their respective luminal surfaces during proestrus and estrus.

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Basic fibroblast growth factor induces 3T3 fibroblasts to synthesize and secrete a cyclophilin-like protein and β2-microglobulin

Cited by 49 publications

References 26 publications

Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes

Role of cyclophilin A in the uptake of HIV-1 by macrophages and T lymphocytes

Dexamethasone-induced expression of the glucocorticoid response gene lipocalin 2 in chondrocytes

Ovarian steroids regulate 24p3 expression in mouse uterus during the natural estrous cycle and the preimplantation period

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