Both Platelet-Derived Growth Factor Receptor (PDGFR)-α and PDGFR-β Promote Murine Fibroblast Cell Migration

Yu, Jiuhong; Moon, Aree; Kim, Hyeong Reh Choi

doi:10.1006/bbrc.2001.4622

Cited by 79 publications

(63 citation statements)

References 17 publications

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“…This involves a complex interplay of growth factors and cytokines and multiple cell types including fibroblasts (1). The PDGF family has long been recognized as a key player in the process of wound healing, and PDGF-R␣ mediates the proliferation (7) and migration (8) of fibroblasts. PDGF-R␣ is induced during wound healing (10,36), and PDGF-R␣-null mice display severe skin abnormalities (9).…”

Section: Discussionmentioning

confidence: 99%

“…For example, PDGF-R␣ is important in gastrulation and the development of the cranial and cardiac neural crest, lung, skin, skeleton, and central nervous system, whereas PDGF-R␤ signaling mediates blood vessel formation and early hematopoiesis (6). PDGF-R␣ mediates fibroblast proliferation (7) and migration (8), and PDGF-R␣-deficient mice knockouts display dermal defects. PDGF-R␣-null mice have severe dermal mesenchymal hypoplasia and skin blistering (9).…”

Section: Pdgf-r␣/␣ and Pdgfr-␣/␤ Pdgf-dd Activates Pdgf-r␤/␤ And Pdgmentioning

confidence: 99%

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Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

Zhang

Khachigian

2009

Journal of Biological Chemistry

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Section: Discussionmentioning

confidence: 99%

Section: Pdgf-r␣/␣ and Pdgfr-␣/␤ Pdgf-dd Activates Pdgf-r␤/␤ And Pdgmentioning

confidence: 99%

Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

Zhang

Khachigian

2009

Journal of Biological Chemistry

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“…PDGF action is directed to PDGFa and -b receptors with tyrosin kinase activity that are present on the surface of stimulated fibroblasts. 75 The fibrotic activity of TGFb and bFGF seems to depend on PDGF pro-fibrotic activity. Indeed, in experimental models PDGF was shown to be essential for desmoplastic response.…”

Section: Possible Mechanisms Of Fibroblast Activationmentioning

confidence: 99%

The pathology of tumor stromatogenesis

Giatromanolaki¹,

Sivridis²,

Koukourakis³

2007

Cancer Biology & Therapy

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Stromatogenesis is the formation of new, specific type, stroma at sites of active tumor cell invasion as an integral part of the invading process. The newly formed stroma by being wedged between tissue planes of least resistance disrupts the continuity of normal structures cleaving paths for the invading tumor cells-intramural stromatogenesis for endophytic tumors. Less frequently, the new stroma is formed towards a void space, i.e., at the free surfaces, whether internal or external (extramural stromatogenesis for exophytic tumors). It is postulated that the formation of this new stroma is generated and governed by the invading tumor cells with the tolerance and complicity of the adjacent activated fibroblasts. The spindle cells of the "neostroma" are intensely proliferating myofibroblasts, which are characterized by the frequent expression of a-smooth muscle actin and the particularly frequent expression of thymidine phosphorylase, PDGF-receptors and SPARC (secreted protein acidic rich in cysteine). The cellular and extracellular qualities, different as they are from those of reactive fibrosis, make stromatogenesis amenable to easy penetration by neoplastic cells and a prospective method for diagnosing early tumor invasion. Studies also suggest that the neostroma has complementary to cancer cell metabolic activity, important for buffering of cancer cell waste products and for the prevention of cancer cell acidic death. Thus, cancer cells and neostroma should not be seen as a mixture of heterogeneous uncoordinated cells but rather as a unified morphologic and metabolic domain with a harmonious collaboration between aerobic (myofibroblasts, endothelial cells) and anaerobic compartments (cancer cells).

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“…The data presented here strongly suggest that an autocrine loop fuels ovarian cancer cell proliferation. Aside from proliferation, the activated receptor modulates other processes significant to tumor expansion (migration (Yu et al, 2001), invasion, stroma modulation (Franklin et al, 1990;Pietras et al, 2002;Dong et al, 2004), etc. ); however, these effects were not examined in the current report.…”

Section: )mentioning

confidence: 99%

“…They are implicated in a variety of physiologic and pathologic processes, including cell growth and survival (Yao and Cooper, 1995), transformation (Huang et al, 1984), migration (Uren et al, 1994;Yu et al, 2001), vascular permeability, stroma modulation and wound healing (Greenhalgh et al, 1990). PDGF binds selectively to receptor subunits, based on specific epitopes (Jensen et al, 1992;Yu et al, 1994); PDGF AA binds the PDGFRa, whereas PDGF AB and BB recognize both the PDGFRa and b (Hart et al, 1988).…”

Section: Introductionmentioning

confidence: 99%

Autocrine activation of PDGFRα promotes the progression of ovarian cancer

et al. 2005

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Platelet-derived growth factor receptor (PDGFR)a expression was found in ovarian cancer cells and tumors by microarray hybridization. This led us to test whether ovarian cancers also produce ligands for this receptor, as this would demonstrate that such malignancies support their own growth and spread through autocrine activation. We assayed the expression of ligands for the PDGFR in ovarian tumors, cell lines and peritoneal fluid using RT-PCR, immunohistochemistry (IHC) and ELISA. We detected strong mRNA expression for the PDGFRa ligands in most ovarian tumors. Receptor and ligand expressions (PDGFRa and PDGF AB) were also detected by IHC in, respectively, 34 and 32 of 47 ovarian tumors. The stainings for PDGFRa and PDGF AB were strongly correlated (P-value ¼ 0.014), suggesting that an autocrine loop is functional in ovarian cancer. PDGF AA and BB were quantified in peritoneal fluid by ELISA. Both ligands are secreted at higher levels in ovarian cancer ascites specimens (n ¼ 54) than in fluid from nonmalignant disorders (n ¼ 8). PDGF was detected in media conditioned by ovarian cancer cells. Such conditioned media induced activation of the PDGFR, Akt and MAPK and stimulated cell proliferation. A neutralizing PDGF antibody blocked these effects. Specific PDGFR inhibition by siRNA or a neutralizing antibody to the receptor inhibited PDGF-stimulated receptor activation and cell proliferation, suggesting that receptor targeting has a role in ovarian cancer treatment.

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Both Platelet-Derived Growth Factor Receptor (PDGFR)-α and PDGFR-β Promote Murine Fibroblast Cell Migration

Cited by 79 publications

References 17 publications

Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

Injury-induced Platelet-derived Growth Factor Receptor-α Expression Mediated by Interleukin-1β (IL-1β) Release and Cooperative Transactivation by NF-κB and ATF-4

The pathology of tumor stromatogenesis

Autocrine activation of PDGFRα promotes the progression of ovarian cancer

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