Phenotypic transformation of normal rat kidney cells by transforming growth factor β is not paralleled by enhanced production of a platelet‐derived growth factor

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Abstract
Phenotypic transformation of normal rat kidney (NRK) cells requires the concerted action of multiple polypeptide growth factors. Serum‐deprived NRK cells cultured in the presence of epidermal growth factor (EGF) become density‐inhibited at confluence, but they can be restimulated by a number of defined polypeptide growth factors, resulting in phenotypic cellular transformation. Kinetic data show that restimulation by transforming growth factor β (TGF‐β) and retinoic acid is delayed when compared to induction by platelet‐derived growth factor (PDGF), indicating that both TGFβ and retinoic acid may exert their growth‐stimulating action by an indirect mechanism. Northern blot analysis shows that NRK cells express the genes for various polypeptide growth factors, including TGFβ1, PDGF A‐chain and basic fibroblast growth factor, but that the levels of expression are not affected by TGFβ or retinoic acid treatment. NRK cells also secrete low amounts of a PDGF‐like growth factor into their extracellular medium, but the levels of secretion are insufficient to induce mitogenic stimulation and are unaffected by agents inducing phenotypic transformation. In combination with studies on the effects of anti‐PDGF antibodies, it is concluded that phenotypic transformation of NRK cells by TGFβ and retinoic acid is not the result of enhanced production of a PDGF‐like growth factor.

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