Leydig cell

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Leydig cell
Leydig cells - very high mag.jpg
Micrograph showing a cluster of Leydig cells (center of image). H&E stain.
Testicle-histology-boar-2.jpg
Histological section through testicular parenchyma of a boar. 1 Lumen of convoluted part of the seminiferous tubules, 2 spermatids, 3 spermatocytes, 4 spermatogonia, 5 Sertoli cell, 6 myofibroblasts, 7 Leydig cells, 8 capillaries
Identifiers
MeSH D007985
FMA 72297
Anatomical terms of microanatomy

Leydig cells, also known as interstitial cells of the testes and interstitial cells of Leydig, are found adjacent to the seminiferous tubules in the testicle and produce testosterone in the presence of luteinizing hormone (LH). [1] [2] They are polyhedral in shape and have a large, prominent nucleus, an eosinophilic cytoplasm, and numerous lipid-filled vesicles. [3]

Contents

Structure

The mammalian Leydig cell is a polyhedral epithelioid cell with a single eccentrically located ovoid nucleus. The nucleus contains one to three prominent nucleoli and large amounts of dark-staining peripheral heterochromatin. The acidophilic cytoplasm usually contains numerous membrane-bound lipid droplets and large amounts of smooth endoplasmic reticulum (SER). [4] Besides the abundance of SER with scattered patches of rough endoplasmic reticulum, several mitochondria are also prominent within the cytoplasm. Reinke crystals have lipofuscin pigment and rod-shaped crystal-like structures 3 to 20 micrometres in diameter. [5]

Adult-type Leydig cells differentiate in the post-natal testis and are dormant until puberty. [6] They are preceded in the testis by a population of fetal-type Leydig cells from the 8th to the 20th week of gestation, which produce enough testosterone for masculinisation of a male fetus. [7]

Androgen production

Leydig cells release a class of hormones called androgens (19-carbon steroids). [8] They secrete testosterone, androstenedione and dehydroepiandrosterone (DHEA), when stimulated by the luteinizing hormone (LH), which is released from the anterior pituitary in response to gonadotropin releasing hormone which in turn is released by the hypothalamus. [8]

LH binds to its receptor (LHCGR) which is a G-protein coupled receptor and consequently increases the production of cAMP. [8] cAMP, in turn through protein kinase A activation, stimulates cholesterol translocation from intracellular sources (primarily the plasma membrane and intracellular stores) to the mitochondria, firstly to the outer mitochondrial membrane and then cholesterol needs to be translocated to the inner mitochondrial membrane by steroidogenic acute regulatory protein, which is the rate-limiting step in steroid biosynthesis. This is followed by pregnenolone formation from the translocated cholesterol via the cholesterol side-chain cleavage enzyme, which is found in the inner mitochondrial membrane, eventually leading to testosterone synthesis and secretion by Leydig cells. [8]

In rats, prolactin (PRL) increases the response of Leydig cells to LH by increasing the number of LH receptors expressed on Leydig cells. [9]

Clinical significance

Micrograph of a Leydig cell tumour. H&E stain. Leydig cell tumour3.jpg
Micrograph of a Leydig cell tumour. H&E stain.

Leydig cells may grow uncontrollably and form a Leydig cell tumour. These may be hormonally active, i.e. secrete testosterone. The function of Reinke crystals is unknown, but they appear in the case of Leydig cell tumours. [5] They are found in less than half of all Leydig cell tumors, but when present, they may serve to confirm the diagnosis of a Leydig cell tumor. [10] [11] No other interstitial cell within the testes has a nucleus or cytoplasm with these characteristics, making identification relatively easy.

While any age is susceptible to a Leydig cell tumour, Leydig cell tumours are more common in people aged 5 to 10 and 30 to 35. [12] A Leydig cell tumour in a child usually causes precocious puberty. [12] About 10% of boys with the tumour have gynecomastia. [12] Although a Leydig cell tumour is always benign in children, it is malignant in 10% to 15% of adults. [12] It is the most common testicular cancer of non-germ cell origin. [13]

Sonography may be used to identify cystic areas, but it is unable to tell benign tumours apart from malignant tumours. [13]

Adrenomyeloneuropathy is another example of a disease affecting the Leydig cell. [14] In this case, a person's testosterone may fall despite higher-than-normal levels of LH and follicle-stimulating hormone (FSH).

Etymology

Leydig cells are named after the German anatomist Franz Leydig, who discovered them in 1850. [15]

Additional images

See also

Related Research Articles

<span class="mw-page-title-main">Testicle</span> Internal organ in the male reproductive system

A testicle or testis is the male gonad in all bilaterians, including humans. It is homologous to the female ovary. The functions of the testicles are to produce both sperm and androgens, primarily testosterone. Testosterone release is controlled by the anterior pituitary luteinizing hormone, whereas sperm production is controlled both by the anterior pituitary follicle-stimulating hormone and gonadal testosterone.

<span class="mw-page-title-main">Androgen</span> Any steroid hormone that promotes male characteristics

An androgen is any natural or synthetic steroid hormone that regulates the development and maintenance of male characteristics in vertebrates by binding to androgen receptors. This includes the embryological development of the primary male sex organs, and the development of male secondary sex characteristics at puberty. Androgens are synthesized in the testes, the ovaries, and the adrenal glands.

<span class="mw-page-title-main">Luteinizing hormone</span> Gonadotropin secreted by the adenohypophysis

Luteinizing hormone is a hormone produced by gonadotropic cells in the anterior pituitary gland. The production of LH is regulated by gonadotropin-releasing hormone (GnRH) from the hypothalamus. In females, an acute rise of LH known as an LH surge, triggers ovulation and development of the corpus luteum. In males, where LH had also been called interstitial cell–stimulating hormone (ICSH), it stimulates Leydig cell production of testosterone. It acts synergistically with follicle-stimulating hormone (FSH).

<span class="mw-page-title-main">Spermatogenesis</span> Production of sperm

Spermatogenesis is the process by which haploid spermatozoa develop from germ cells in the seminiferous tubules of the testicle. This process starts with the mitotic division of the stem cells located close to the basement membrane of the tubules. These cells are called spermatogonial stem cells. The mitotic division of these produces two types of cells. Type A cells replenish the stem cells, and type B cells differentiate into primary spermatocytes. The primary spermatocyte divides meiotically into two secondary spermatocytes; each secondary spermatocyte divides into two equal haploid spermatids by Meiosis II. The spermatids are transformed into spermatozoa (sperm) by the process of spermiogenesis. These develop into mature spermatozoa, also known as sperm cells. Thus, the primary spermatocyte gives rise to two cells, the secondary spermatocytes, and the two secondary spermatocytes by their subdivision produce four spermatozoa and four haploid cells.

<span class="mw-page-title-main">Sertoli cell</span> Cells found in human testes which help produce sperm

Sertoli cells are a type of sustentacular "nurse" cell found in human testes which contribute to the process of spermatogenesis as a structural component of the seminiferous tubules. They are activated by follicle-stimulating hormone (FSH) secreted by the adenohypophysis and express FSH receptor on their membranes.

<span class="mw-page-title-main">Brenner tumour</span> Medical condition

Brenner tumours are an uncommon subtype of the surface epithelial-stromal tumour group of ovarian neoplasms. The majority are benign, but some can be malignant.

<span class="mw-page-title-main">Sertoli–Leydig cell tumour</span> Medical condition

Sertoli–Leydig cell tumour is a group of tumors composed of variable proportions of Sertoli cells, Leydig cells, and in the case of intermediate and poorly differentiated neoplasms, primitive gonadal stroma and sometimes heterologous elements.

<span class="mw-page-title-main">Sex cord–gonadal stromal tumour</span> Medical condition

Sex cord–gonadal stromal tumour is a group of tumours derived from the stromal component of the ovary and testis, which comprises the granulosa, thecal cells and fibrocytes. In contrast, the epithelial cells originate from the outer epithelial lining surrounding the gonad while the germ cell tumors arise from the precursor cells of the gametes, hence the name germ cell. In humans, this group accounts for 8% of ovarian cancers and under 5% of testicular cancers. Their diagnosis is histological: only a biopsy of the tumour can make an exact diagnosis. They are often suspected of being malignant prior to operation, being solid ovarian tumours that tend to occur most commonly in post menopausal women.

<span class="mw-page-title-main">Spermatocyte</span> Sperm precursor cell that undergoes meiosis

Spermatocytes are a type of male gametocyte in animals. They derive from immature germ cells called spermatogonia. They are found in the testis, in a structure known as the seminiferous tubules. There are two types of spermatocytes, primary and secondary spermatocytes. Primary and secondary spermatocytes are formed through the process of spermatocytogenesis.

<span class="mw-page-title-main">Male reproductive system</span> Reproductive system of the human male

The male reproductive system consists of a number of sex organs that play a role in the process of human reproduction. These organs are located on the outside of the body, and within the pelvis.

The steroidogenic acute regulatory protein, commonly referred to as StAR (STARD1), is a transport protein that regulates cholesterol transfer within the mitochondria, which is the rate-limiting step in the production of steroid hormones. It is primarily present in steroid-producing cells, including theca cells and luteal cells in the ovary, Leydig cells in the testis and cell types in the adrenal cortex.

<span class="mw-page-title-main">Luteinizing hormone/choriogonadotropin receptor</span> Transmembrane receptor found in humans

The luteinizing hormone/choriogonadotropin receptor (LHCGR), also lutropin/choriogonadotropin receptor (LCGR) or luteinizing hormone receptor (LHR), is a transmembrane receptor found predominantly in the ovary and testis, but also many extragonadal organs such as the uterus and breasts. The receptor interacts with both luteinizing hormone (LH) and chorionic gonadotropins and represents a G protein-coupled receptor (GPCR). Its activation is necessary for the hormonal functioning during reproduction.

<span class="mw-page-title-main">Germ cell neoplasia in situ</span> Medical condition

Germ cell neoplasia in situ (GCNIS) represents the precursor lesion for many types of testicular germ cell tumors.

<span class="mw-page-title-main">Sertoli cell tumour</span> Medical condition

A Sertoli cell tumour, also Sertoli cell tumor, is a sex cord–gonadal stromal tumour of Sertoli cells. They can occur in the testis or ovary. They are very rare and generally peak between the ages of 35 and 50. They are typically well-differentiated and may be misdiagnosed as seminomas as they often appear very similar.

<span class="mw-page-title-main">Leydig cell tumour</span> Medical condition

Leydig cell tumour, also Leydig cell tumor, (testicular) interstitial cell tumour and (testicular) interstitial cell tumor, is a member of the sex cord-stromal tumour group of ovarian and testicular cancers. It arises from Leydig cells. While the tumour can occur at any age, it occurs most often in young adults.

<span class="mw-page-title-main">Leydig cell hypoplasia</span> Medical condition

Leydig cell hypoplasia (LCH), also known as Leydig cell agenesis, is a rare autosomal recessive genetic and endocrine syndrome affecting an estimated 1 in 1,000,000 genetic males. It is characterized by an inability of the body to respond to luteinizing hormone (LH), a gonadotropin which is normally responsible for signaling Leydig cells of the testicles to produce testosterone and other androgen sex hormones. The condition manifests itself as pseudohermaphroditism, hypergonadotropic hypogonadism, reduced or absent puberty, and infertility.

Follicle-stimulating hormone (FSH) insensitivity, or ovarian insensitivity to FSH in females, also referable to as ovarian follicle hypoplasia or granulosa cell hypoplasia in females, is a rare autosomal recessive genetic and endocrine syndrome affecting both females and males, with the former presenting with much greater severity of symptomatology. It is characterized by a resistance or complete insensitivity to the effects of follicle-stimulating hormone (FSH), a gonadotropin which is normally responsible for the stimulation of estrogen production by the ovaries in females and maintenance of fertility in both sexes. The condition manifests itself as hypergonadotropic hypogonadism, reduced or absent puberty, amenorrhea, and infertility in females, whereas males present merely with varying degrees of infertility and associated symptoms.

Reinke crystals are rod-like cytoplasmic inclusions which can be found in Leydig cells of the testes. Occurring only in adult humans and wild bush rats, their function is unknown.

<span class="mw-page-title-main">Vassilios Papadopoulos</span>

Vassilios Papadopoulos, DPharm, PhD, DSc (hon), born February 18, 1961, in Athens, Greece, is a scholar, researcher, inventor, professor, and university administrator who has served as dean of the USC Alfred E. Mann School of Pharmacy and Pharmaceutical Sciences at the University of Southern California in Los Angeles, California, since 2016. Previously, he was the associate vice president and director of the Biomedical Graduate Research Organization at Georgetown University from 2005 to 2007, and the executive director and chief scientific officer of the Research Institute of the McGill University Health Center from 2007 to 2015.

<span class="mw-page-title-main">Peritubular myoid cell</span> Smooth muscle cell found in testis

A peritubular myoid (PTM) cell is one of the smooth muscle cells which surround the seminiferous tubules in the testis. These cells are present in all mammals but their organization and abundance varies between species. The exact role of PTM cells is still somewhat uncertain and further work into this is needed. However, a number of functions of these cells have been established. They are contractile cells which contain actin filaments and are primarily involved in transport of spermatozoa through the tubules. They provide structural integrity to the tubules through their involvement in laying down the basement membrane. This has also been shown to affect Sertoli cell function and PTM cells also communicate with Sertoli cells through the secretion of growth factors and ECM components. Studies have shown PTM cells to be critical in achieving normal spermatogenesis. Overall, PTM cells have a role in both maintaining the structure of the tubules and regulating spermatogenesis through cellular interaction.

References

  1. ↑ Chabner, Davi-Ellen (2016). The Language of Medicine - E-Book. Elsevier Health Sciences. p. 316. ISBN   978-0-32-337083-7.
  2. ↑ Johnson, Martin H. (2018). Essential Reproduction. John Wiley & Sons. p. 131. ISBN   978-1-11-924645-9.
  3. ↑ Zhou, Ming; Netto, George; Epstein, Jonathan I (2022). Uropathology E-Book. Elsevier Health Sciences. p. 428. ISBN   978-0-32-365396-1.
  4. ↑ Rhoades, Rodney A.; Bell, David R. (2022). Medical Physiology: Principles for Clinical Medicine. Lippincott Williams & Wilkins. p. 2031. ISBN   978-1-97-516045-6.
  5. 1 2 Partin, Alan W.; Wein, Alan J.; Kavoussi, Louis R.; Peters, Craig A.; Dmochowski, Roger R. (2020). Campbell Walsh Wein Urology. Elsevier Health Sciences. p. 1124. ISBN   978-0-32-367227-6.
  6. ↑ Nieschlag, Eberhard; Behre, Hermann M. (2012). Testosterone: Action - Deficiency - Substitution. Springer Science & Business Media. p. 9. ISBN   978-3-64-272185-4.
  7. ↑ Svechnikov K, Landreh L, Weisser J, Izzo G, Colón E, Svechnikova I, Söder O (2010). "Origin, development and regulation of human Leydig cells". Horm Res Paediatr. 73 (2): 93–101. doi: 10.1159/000277141 . PMID   20190545. S2CID   5986143.
  8. 1 2 3 4 Zirkin, Barry R; Papadopoulos, Vassilios (July 2018). "Leydig cells: formation, function, and regulation". Biology of Reproduction. 99 (1): 101–111. doi:10.1093/biolre/ioy059. ISSN   0006-3363. PMC   6044347 . PMID   29566165.
  9. ↑ Steinbach, Thomas J.; Patrick, Daniel J.; Cosenza, Mary Ellen (2019). Toxicologic Pathology for Non-Pathologists. Springer Nature. p. 1124. ISBN   978-1-49-399777-0.
  10. ↑ Al-Agha O, Axiotis C (2007). "An in-depth look at Leydig cell tumor of the testis". Arch Pathol Lab Med. 131 (2): 311–7. doi:10.5858/2007-131-311-AILALC. PMID   17284120.
  11. ↑ Ramnani, Dharam M (2010-06-11). "Leydig Cell Tumor : Reinke's Crystalloids" . Retrieved 2011-11-06.
  12. 1 2 3 4 Jameson, J. Larry; De Groot, Leslie J. (2015). Endocrinology: Adult and Pediatric. Elsevier Health Sciences. p. 2365. ISBN   978-0-32-332195-2.
  13. 1 2 Henningsen, Charlotte; Kuntz, Kathryn; Youngs, Diane (2013). Clinical Guide to Sonography: Exercises for Critical Thinking. Elsevier Health Sciences. p. 350. ISBN   978-0-32-309164-0.
  14. ↑ Chovel-Sella, Alum; Halper, Alyssa (2020). "Adrenal Insufficiency". Endocrine Conditions in Pediatrics: A Practical Guide. Springer Nature. p. 286. ISBN   978-3-03-052215-5.
  15. ↑ synd/625 at Who Named It?

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