Regenerating I messenger RNA and protein expression in the failing human testis: a potential molecular prognostic marker of seminoma.

Infertility has been stated as a risk factor for testicular cancer; but currently, there is no prognostic indicator of tumor development from the pathologic testis with impaired spermatogenesis. Regenerating proteins are expressed in many human tissues including the testis, and their role in carcinogenesis has been well documented. In the present work, regenerating I messenger RNA and protein expression and cellular protein localization were studied in testicular biopsies of patients with normal (obstructive azoospermia) or impaired spermatogenesis (nonobstructive azoospermia) and in seminoma testis by quantitative reverse transcriptase-polymerase chain reaction, Western blot, and immunofluorescence analyses.

Reg I protein in healthy and seminoma human testis.

Regenerating gene (Reg), encodes a secretory protein with growth and differentiation stimulating effects mostly in digestive tissues. Overexpression of Reg proteins and specifically of Reg I, one member of the Reg family, is associated with several human diseases and cancers. In the present study we analyzed the expression of Reg I in normal rodent and human testes where germ cells normally proliferate and differentiate into spermatozoa, and in seminoma testis, the most common cancer of young men.

A potential novel mechanism involving connexin 43 gap junction for control of sertoli cell proliferation by thyroid hormones.

There is strong evidence that thyroid hormones through triiodothyronine (T3) regulate Sertoli cell proliferation and differentiation in the neonatal testis. However, the mechanism(s) by which they are able to control Sertoli cell proliferation is unclear. In the present study in vivo approaches (PTU-induced neonatal hypothyroidism known to affect Sertoli cell proliferation) associated with in vitro experiments on a Sertoli cell line were developed to investigate this question.

Trophic status of the small intestine in young and aged rats: modulation by a yogurt-supplemented diet.

Among the multifactorial causes of undernutrition in old age, gastrointestinal mucosa altered function and resulting specific malabsorption are the most relevant. Despite numerous studies that have dealt with the effects of aging on the digestive tract of mammals, results showed discrepancies in terms of proliferation and biochemical aging small intestine events. However, the slowing-down of the maturation process and the poor adaptation of metabolism and intestinal function are obvious and there is evidence that protective mechanisms are impaired with age and contribute to affecting the trophic activity and related systemic homeostasis.

Consequences of adrenalectomy on small intestine trophic parameters in aged and young rats: evidence of defective adaptation by aging and lack of corticoids.

Previous study pointed to an important role of adrenals and glucocorticoids in the trophic status of the adult small intestine mucosa, with possible implications during stress events. Small intestine morphological and biochemical consequences of 10-day bilateral adrenalectomy and also sham-related laparotomy were determined in 23-month-old Sprague-Dawley rats. As described in young rats, adrenalectomy in old rats leads to partial atrophy and disorganization of the proximal small intestine epithelium, with an increase in the number of Paneth cells and reduced crypt cell proliferation.