Studies of parathyroid hormone-like peptide (PLP) have demonstrated that PLP gene expression is inducible by serum, growth factors, and cycloheximide. Rapid induction of PLP gene expression has also been observed following the induction of cell differentiation. These features of PLP gene expression are consistent with a role for PLP in the regulation of cell growth and differentiation. To understand the biology of PLP in developing cells and tissues, we have studied the distribution of PLP gene expression in the fetal and neonatal rat. PLP was localized by immunocytochemistry to skin, vascular smooth muscle, skeletal muscle, heart, liver, kidney, lung, and gastrointestinal tract in Day 14 fetal rat. By Day 18 PLP immunopositivity was also detected in both fetal pituitary and adrenal medulla, as well as in endocrine pancreas. Whereas few PLP-immunopositive cells were detected in Day 14 brain, scattered areas of PLP immunopositivity were evident in Day 18 brain, in regions such as the choroid plexus. Immunostaining for PLP was also detected in Day 18 tissues that were positive on Day 14. The pattern of staining in fetal testis, where PLP was strongly localized to seminiferous tubules, differed from adult testis, where PLP was localized predominantly in Leydig cells. PLP was localized to the hepatocytes but not to the hematopoietic elements in fetal liver. Neonatal hepatocytes were weakly PLP immunopositve, and PLP was not detected in adult rat liver. Northern blot analysis demonstrated the presence of a single 1.4-kilobase PLP mRNA transcript in fetal brain, liver, heart, lung, and intestine. The results of these studies demonstrate that the PLP gene is widely expressed in a diverse number of fetal rat tissues. The cellular and tissue localization of PLP immunopositively remains fairly constant in the transition from fetal to neonatal and adult tissues except in the testis, where a cellular switch in PLP-producing cells occurs, and the liver, where PLP gene expression is progressively extinguished postnatally.


This work was supported in part by operating grants from the Canadian Diabetes Association and the National Cancer Institute of Canada. D. J. D. is a Career Scientist of the Ontario Ministry of Health, and R. V. C. is a recipient of a Medical Research Council of Canada-ICI Pharma Fellowship.

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