Sertoli cell

Sertoli cells are named after Enrico Sertoli, an Italian physiologist who discovered them while studying medicine at the University of Pavia, Italy.[1] He published a description of his eponymous cell in 1865.[2] The cell was discovered by Sertoli with a Belthle microscope which had been purchased in 1862. In the 1865 publication, his first description used the terms "tree-like cell" or "stringy cell"; most importantly, he referred to these as "mother cells". Other scientists later used Enrico's family name to label these cells in publications, beginning in 1888. As of 2006, two textbooks that are devoted specifically to the Sertoli cell have been published.

Sertoli cells are specifically located in the convolutions of the seminiferous tubules, since this is the only place in the testes where spermatozoa are produced. As the primary support cell of the tubules, they are generally very large and amorphous, with individual cells stretching from the basal lamina to the lumen; their cytoplasm often completely surrounds the germline cells which they are responsible for nursing. Sertoli cells are easily confused with the other cells of the germinal epithelium when using standard staining techniques; the most distinctive feature of the Sertoli cell is its dark nucleolus.[3]

Sertoli cells are required for male sexual development. Sertoli cell proliferation and differentiation is mainly activated by FGF9, with which they also form a feedforward loop.[4][5] It has been suggested that Sertoli cells may derive from the fetal mesonephros.[6] After puberty, Sertoli cells begin to elongate. Their nucleoli become larger and tight junctions are completed, creating a fluid-filled lumen space.[7]

FSH is responsible for controlling the proliferation of Sertoli cells shortly after birth and stimulates the production of factors derived from Sertoli cells that control the development of the testes and germ cells. FSH, luteinizing hormone. thyroid-stimulating hormone, and hCG are all known to affect Sertoli cell development and male reproductive health. FSH is required for Sertoli cell mitogen, which stimulates the expression of various cell markers.[7]

Once fully differentiated, the Sertoli cell is considered terminally differentiated, and is unable to proliferate.[8] Therefore, once spermatogenesis has begun, no more Sertoli cells are created, and their population within the seminiferous tubules is finite.

Recently, however, scientists have found a way to induce Sertoli cells to a juvenile proliferative phenotype outside of the body.[9] This gives rise to the possibility of repairing some defects of testicular niche cells which may cause male infertility.

Because its main function is to nourish developing sperm cells through the stages of spermatogenesis, the Sertoli cell has also been called the "mother" or "nurse" cell.[10] Sertoli cells also act as phagocytes, consuming the residual cytoplasm during spermatogenesis. Translocation of cells from the basal lamina to the lumen of the seminiferous tubules occurs by conformational changes in the lateral margins of the Sertoli cells.

Sertoli-Leydig cell tumour is part of the sex cord-stromal tumour group of ovarian neoplasms. These tumors produce both Sertoli and Leydig cells and lead to an increased secretion of testosterone in ovaries and testicles.

Cross-section of a seminiferous tubule of the testis of a rat (250x)

The function of Sertoli cells in the Amniota and Anamniota is the same, but they have slightly different properties when compared to each other. Anamnionts (fish and amphibians) employ cystic spermatogenesis in order to produce sperm cells.[22] In the Amniota, Sertoli cells are terminally differentiated cells which are normally incapable of proliferating. In the Anamniota, Sertoli cells go through two proliferative phases. The first phase of proliferation occurs during cyst establishment, promoting the migration of germ cells into it.[23][24] The second phase involves enlargement of the cyst which produces space for the proliferating germ cells.[25]

The once commonly accepted fact that Sertoli cells are unable to divide and proliferate in Amniota has recently been challenged. Upon xenogenic transplantation, Sertoli cells have been shown to regain the ability to proliferate.[26]

Recently (2016), experimental models of autoimmune inflammatory disorders, including diabetes, have prompted the implication of Sertoli cells into cell therapy transplantation thanks to their immunoregulatory and anti-inflammatory properties.[27]

Research into adapting Sertoli cells for use in the treatment of type I diabetes mellitus involves the strategy of cotransplanting β cells together with Sertoli cells into the recipient organism. In mice, rats, and humans, the presence of these cells restored glucose homeostasis as well as lowered requirements for external insulin. In all cases no immunosuppression was used, and the role of this medication was taken and provided by SC.[28][29][30]

By treating spontaneously diabetic and obese mice with the transplantation of microencapsulated Sertoli cells in subcutaneous abdominal fat deposits, Giovanni et al.[27] demonstrated that more than half of the treated mice showed improved glucose homeostasis. This recent scientific work promises a future better treatment to patients with type 2 diabetes mellitus through the use of cell therapy.

Sertoli cells promote skin graft acceptance by the recipient organism[31] and their presence also helps to increase the numbers of motor neurons in the spinal cord of SOD1 mice (a mouse model used in the study of amyotrophic lateral sclerosis).[32]

• Sertoli cell-only syndrome
• Sertoli cell nodule
• List of distinct cell types in the adult human body

Wikimedia Commons has media related to Sertoli cells.

• Histology image: 17805loa – Histology Learning System at Boston University
• Histology image: 17806loa – Histology Learning System at Boston University