2 However, the concept of Lamarckian inheritance was subsequently rejected. August Weismann, who proposed the theory that characteristics are transmitted only through the germ cells, but not the somatic cells, the so-called germ plasm theory, rebutted see more Lamarckian inheritance.3 He claimed that germ cells are strictly segregated from somatic cells, a separation that came to be referred to as the “Weismann Barrier.” In his theory, the characteristics that somatic cells learned and acquired during their lifetime

could not be transmitted into germ cells, which is inconsistent with Lamarckian inheritance. However, recent progress in epigenetics provided evidence that environmental factors change epigenetic information, such as DNA methylation and histone tail modifications, and the alteration of epigenetic information is indeed inherited beyond the given generation, so-called transgenerational effects.4, 5 Zeybel et al.6 have uncovered that hepatic fibrosis leads to epigenetic changes in the sperm, which exert a suppressive function against fibrosis in subsequent male offspring. Surprisingly, this epigenetic information was transmittable through serum, derived from

MK-1775 purchase fibrotic rats, to normal rats, which implies that memorized epigenetic information can be transmitted across the Weismann Obeticholic Acid research buy barrier, mediated by serum. This report supports Lamarckian inheritance in which the traits acquired from environmental cues can be transmitted to the next generation. The authors focused on the difference in susceptibility in the progression of liver cirrhosis among patients. They hypothesized that ancestral liver damage confers adaptive traits that are transmitted between generations through heritable epigenetic, rather than genetic, changes. They treated F0 and F1 male rats with the hepatotoxin carbon

tetrachloride (CCl4) to induce hepatic injury, and then compared the degree of liver injury and fibrosis in F2 male rats after the administration of CCl4. There were no obvious differences in liver injury, but there was a difference in wound healing among F2 male rats. Male rats whose father and grandfather both had liver injury showed the least fibrosis, male rats whose father and grandfather both did not have liver injury showed the most severe fibrotic phenotype. These results indicate that ancestral liver injury provides heritable characteristics for the suppression of wound healing that occurs after liver injury. Liver fibrosis is caused by the overproduction of collagen derived from myofibroblasts that arise from hepatic stellate cells.