A novel isoform of the β subunit of thyroid stimulating hormone in the human pituitary gland, peripheral blood leukocytes and thyroid gland (2023)

fragments section

Reverse transcriptase PCR (RT-PCR) en kwantitatieve real-time PCR (qRT-PCR)

High purity RNA from human pituitary, bone marrow, peripheral blood leukocytes (PBL), and thyroid tissues was purchased from the BioChain Institute (Hayward, CA) from tissues obtained by informed consent. The primers used were:



Native and novel inverted TSHβ: 5'-AACCAAATTGCAAATTATATCACTA-3'.



The primers were

Identification and tissue expression of an isoform of a human TSHβ splice variant

Two sets of primers were used for analysis of human TSHβ gene expression. One set (designated native TSHβ), designed to amplify the entire human TSHβ open reading frame, consisted of an upstream primer targeting a region in exon 2 before the start site of TSHβ transcription, and a downstream primer targeting a region in exon 3 that begins with a nucleotide after the stop codon. The second set of primers (designated new TSHβ) consisted of an upstream primer targeting a region at the end of the intron.


We believe these findings have important implications for understanding immunoendocrine interactions in a number of ways. The preferential expression of the TSHβ splice variant in PBL and thyroid indicates that immune-derived TSHβ differs significantly from native TSHβ. Based on our studies in mice, which showed that TSHβ-producing myeloid cells migrate to the thyroid gland where they secrete TSH (Klein and Wang, 2004), the likely source of intrathyroidal TSH in the

expressions of gratitude

This work was supported in part by NIH Grants DK035566 and DE015355. The authors thank Dina Montufar-Solis for her expert technical assistance.

Quoted by (23)

  • The splice variant of the thyroid stimulating hormone β subunit is expressed in all fractional subsets of bone marrow hematopoietic cells and peripheral blood leukocytes and is modulated during bacterial infection

    2020, General and Comparative Endocrinology

    Quote excerpt:

    Exceptionally, the 3' end of intron 4 is used to encode the TSHβv signal peptide (Baliram et al., 2013, 2016; Vincent et al., 2009). A molecule similar to mouse TSHβv has been identified in human leukocytes, as well as many different species, and has been associated with Hashimoto's thyroiditis (HT) and thyroid tissue destruction (Liu et al., 2012, 2019, 2015; Schaefer and Klein, 2009). What is not clear is how TSHβv functionally contributes to the overall health and disease of the organism.

    Thyroid stimulating hormone (TSH), a hormone produced in the anterior pituitary gland, is used to regulate thyroid hormone secretion. It has been known for more than three decades that cells of the immune system produce TSH; however, the functional role of TSH in the immune system is unclear. We have previously shown that an alternatively spliced ​​TSHβ isoform, termed the TSHβ splice variant (TSHβv), is the major form of TSHβ produced by hematopoietic cells in mice and humans. Most studies have linked TSHβv expression to myeloid cells of the immune system; however, plasma cells in Hashimoto's thyroiditis patients have recently been shown to be a source of TSHβv for the immune system. Here we show that TSHβv is expressed in bone marrow progenitors of lymphoid cells, monocytes and granulocytes, as well as cells of the mesenteric lymph nodes (MLN). Plasma cells generated by in vitro culture with bacterial lipopolysaccharide (LPS) and MLN cells from mice infected withL. monocytogenesexpressed TSHβv. There was an increase in the intensity of intracellular TSHβv expression in MLN cells after exposure to LPS, and in the ratio of TSHβv+CD138+MLN cell trackingL. monocytogenesinfection. The number of TSHβv+cells were increased in MLN cells, especially in CD138+cells, after a bacterial infection. This was confirmed by an increase in gene expression of BLIMP-1, the transcription factor for CD138, after infection. Circulating thyroxine levels decreased significantly in mice 24 hours after infection. These findings suggest that immune system TSHβv may contribute to the host immune response during bacterial infection.

  • thyroid stimulating hormone

    2017, The Pituitary Gland: Fourth Edition

    Thyroid stimulating hormone (TSH) is a glycoprotein produced by thyrotrophic cells of the anterior pituitary gland and consists of a heterodimer of two non-covalently linked subunits, α and β. Each subunit is encoded by a separate gene located on a different chromosome and is transcribed in a coordinated manner in response to primarily stimulation by thyrotropin-releasing hormone (TRH) and inhibition by thyroid hormone. The production of bioactive TSH involves a process of cotranslational glycosylation and folding that allows the combination between the nascent α and β subunits. TSH is stored in secretory granules and released into the circulation in a regulated manner, primarily in response to TRH stimulation. Circulating TSH binds to specific cell surface receptors in the thyroid gland, where it stimulates the production of thyroid hormone, which modulates many metabolic processes and inhibits TSH production. Sensitive TSH assays provide accurate measurement of circulating TSH levels. Acquired and congenital disorders of TSH production are rare causes of abnormal thyroid function, but it is important to recognize them as a possible cause of abnormal thyroid function tests.

  • Functional human TSHβ splice variant produced by plasma cells may be involved in immune damage to the thyroid in the patient with Hashimoto's thyroiditis

    2015, Molecular and Cellular Endocrinology

    Quote excerpt:

    The novel TSHβ splice variant may play an important role in immunothyroid interaction. Schäfer et al. found a similar splice variant of TSHβ in humans. (Schäfer and Klein, 2009). The human TSHβ splice variant (hTSHβ) consists of a 27-nucleotide portion of intron 2 and the entire exon 3 of the human TSHβ gene.

    Hashimoto's thyroiditis (HT) is the most common cause of hypothyroidism in parts of the world where iodine levels are adequate. However, the pathogenesis of HT has not been fully elucidated. The first functional splice variant of human TSHβ was hypothesized to be involved in the pathology of Hashimoto's thyroiditis. The question remains which type of intrathyroid cells express the functional TSHβ splicing variant and whether there are variations in the expression of the functional TSHβ splicing variant in the damaged thyroid gland of the HT patient. To answer this question, immune-damaged thyroids were obtained from 30 patients with AHT. The study of the location of the functional TSHβ cleavage variant in the damaged thyroid gland was performed using double immunofluorescence staining. The transcription and translation level of functional TSHβ splice variant was detected by qRT-PCR and semiquantitative immunohistochemistry method, respectively. The correlation between the expression level of the functional TSHβ splice variant and the extent of thyroid follicle damage was evaluated.

    First, it was found that the functional TSHβ splice variant is mainly expressed in infiltrated plasma cells surrounding the follicles and germinal center in the damaged thyroid gland of HT patients. Of particular interest was that the TSHβ splice variant was expressed at significantly higher levels in the thyroid tissues of HT patients than in normal thyroid tissues, in addition, the level of expression of the TSHβ splice variant was positively related to the degree of damage to the thyroid follicles of patients with AHT.

    These findings defined the immune system-derived functional splice variant of TSHβ in the thyroid gland of the HT patient, which exerted unique effects on the pathogenesis of HT. Meanwhile, we believe these findings have significant implications for understanding the immunoendocrine interactions in a number of ways. .

  • Thyroid stimulating hormone: physiology and secretion

    2015, Endocrinology: Adult and Pediatric

  • A novel function of lamb and pork: Different effects of lamb and pork consumption on thyroid hormone levels and energy metabolism of Sprague-Dawley rats

    2014, International Food Research

    Quote excerpt:

    The aim of this study was to determine whether consumption of different meats (mutton and pork) had different effects on serum thyroid hormone concentrations and energy metabolism in rats than on casein, to determine if and how certain meats occur. to induce various thermal effects in humans. In this study, results indicated that different diets did not have different effects on TH via the pituitary gland, which secretes TSH by stimulating thyroid function (Schaefer & Klein, 2009). This result is also in agreement with our previous study (Feng et al., 2011).

    Different effects of lamb and pork consumption on thyroid hormone levels and energy metabolism in rats were investigated. Three diets, a lamb diet (LD), a pig diet (PD) and a casein control diet (CD) were isocaloric (15.5 kJ/g dry matter). Rats in the PD group had higher serum selenium concentrations (PAG<0.05) and liver 5'-deiodinase activities (PAG<0.05), caused by a higher selenium content in pork (PM). As a result, PM consumption increased serum triiodothrionine (T3) concentrations (PAG<0.05) and decreased serum thyroxine (T4) concentrations compared to casein and lamb (LM). Compared to casein and LM powder, PM powder had higher total levels of glutamic acid, leucine, aspartic acid, serine, and alanine (48.94 vs. 44.24 vs. 44.78), leading to higher serum concentrations of TBG (PAG<0.05) in the PD group. Compared to casein, PM powder had a higher total leucine and isoleucine content (9.87 vs. 9.21; 5.12 vs. 4.74), LM powder had a lower leucine content (8.14 vs. 9.21), which led to higher serum albumin concentrations in the PD group (PAG<0.05) and lower in the LD group (PAG<0.05). Consequently, the PD group had lower serum concentrations of free T4 (FT4) and free T3 (FT3) (PAG<0.05), which significantly reduced the rats' energy expenditure, while the LD group had higher serum FT3 concentrations (PAG<0.05), which significantly increases energy consumption. These were inferred from the various changes in liver and skeletal muscle Na,K-ATPase activities (PAG<0.05), Oxygen Demand (OCR) (PAG<0.05) and rectal temperature, especially on day 13 (PAG<0.05) and body weights (PAG<0.05) in the PD or LD group. We conclude that the consumption of PM or LM, with a different amino acid composition, had different effects on rat energy metabolism through the multistep regulation of TH.

  • Effect of duck meat consumption on thyroid hormone concentrations and energy metabolism in Sprague-Dawley rats.

    2013, Appetite

    Quote excerpt:

    The aim of this study was to determine whether duck meat consumption affected serum thyroid hormone concentrations and energy metabolism in rats compared to a DC where the major protein component was casein, to determine whether and how certain foods appear to cause different thermal effects . effects in humans. In this study, the results indicated that the two diets did not have different effects on TH via the pituitary gland, which secretes TSH by stimulating thyroid function (Schaefer & Klein, 2009). Dietary selenium concentrations may influence serum thyroid hormone concentrations by regulating the activities of 5'-deiodinase (Buettner, Harney, & Larsen, 1998; Davey, Schneider, Becker, & Galton, 1999), which is responsible for the conversion of T4 in T3 in peripheral tissues (Bates & Spate, 2000; Korytkowski & Kuffner, 2007; LaFranchi, 2006).

    The two diets, a duck meat diet (DMD) and a control casein diet (CD), were isocaloric (15.9 kJ/g dry matter) and contained 18.3% protein, 7.4% fat and 60.0% carbohydrates. The selenium contents in casein, duck meat powder, CD and DMD were 0.061, 0.549, 0.123 and 0.225 mg/kg. Rats in the DMD group had higher serum selenium concentrations (pag<0.05) and liver 5'-deiodinase activities (pag<0.05). As a result, duck meat consumption increased serum concentrations of triiodothrionine (T3) (pag<0.05) and decreased serum thyroxine (T4) concentrations (pag<0.05). The lowest serum concentrations of T4 (pag<0.05) were also supported by the lower total tyrosine and phenylalanine content in duck meat powder compared to casein (7.72 versus 10.13). Compared to casein, duck meat powder had higher total levels of glutamic acid, leucine, aspartic acid, serine and alanine (44.68 vs. 49.21), leading to higher serum concentrations of TBG (pag<0.05) in the DMD group. Therefore, the DMD group had lower serum free T4 (FT4) concentrations (pag<0.05), and lower serum free T3 (FT3) concentrations at day 14 (pag<0.05), which significantly reduced the energy expenditure of rats in the DMD group, with lower Na, K-ATPase and Ca-ATPase activities in the liver (pag<0.05), lower OCR and rectal temperature, especially on day 13 (pag<0.05), higher body weight (pag<0.05) and weight gain (pag<0.05). We conclude that duck meat consumption decreased energy metabolism in rats by regulating TH multisteps.

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Copyright © 2009 Elsevier Inc. All rights reserved.


What is the subunit of the thyroid stimulating hormone beta? ›

Thyroid stimulating hormone consists of two subunits called alpha and beta. The TSHB gene provides instructions for making the beta subunit. The alpha and beta subunits are bound together to produce the active form of the hormone.

What is the thyroid stimulating hormone of the pituitary gland? ›

The pituitary gland makes thyroid stimulating hormone (TSH). TSH tells your thyroid how much thyroid hormone it needs to make. If the thyroid hormone levels in your blood are too low, your pituitary gland makes larger amounts of TSH to tell your thyroid to work harder.

What is the TSH thyroid stimulating hormone? ›

Thyroid-stimulating hormone, commonly called TSH and also referred to as thyrotropin, is a hormone that your pituitary gland releases to trigger your thyroid to produce and release its own hormones — thyroxine (T4) and triiodothyronine (T3).

What hypothalamic and pituitary hormones regulate thyroid hormone T3 T4 secretion? ›

Your hypothalamus releases thyrotropin-releasing hormone (TRH), which triggers your pituitary gland to release thyroid-stimulating hormone (TSH), which stimulates your thyroid to release T3 and T4.

What are T3 T4 thyroid gland hormones? ›

T3 is one of two major hormones made by your thyroid, a small, butterfly-shaped gland located near the throat. The other hormone is called thyroxine (T4.) T3 and T4 work together to regulate how your body uses energy.

What are alpha and beta subunits of pituitary gland? ›

Pituitary glycoprotein hormones are composed of two different subunits, the alpha- and beta-subunits. The alpha-subunit is common to all FSH, LH, and TSH, while the beta-subunit is specific for each of these hormones. We studied the effects of a potent LHRH antagonist on alpha-subunit and LH secretion in normal men.

What does the pituitary gland do with TSH? ›

The pituitary is an endocrine gland located at the base of your brain that controls your endocrine system, including your thyroid. The pituitary affects the thyroid by producing a hormone called thyroid stimulating hormone (TSH). TSH causes cells within your thyroid to make more T3 and T4 hormone.

What is the function of the pituitary gland the thyroid gland? ›

The pituitary gland is referred to as the “master gland” because it monitors and regulates many bodily functions through the hormones that it produces, including: Growth and sexual/reproductive development and function. Glands (thyroid gland, adrenal glands, and gonads) Organs (kidneys, uterus, and breasts)

What does the pituitary gland do to the thyroid gland? ›

The pituitary secretes thyroid stimulating hormone (TSH), which stimulates the thyroid gland to secrete hormones that affect body metabolism.

What level of TSH indicates hypothyroidism? ›

In general, TSH results indicate the following: TSH levels over 10mU/L indicate overt hypothyroidism. People will usually need thyroxine (T4) replacement therapy. TSH levels between 4.5 and 10 mU/L indicate mildly underactive (subclinical) hypothyroidism.

What TSH level means hypothyroidism? ›

Ultimately, the standard of care is to treat into the goal range for TSH, which is typically between 0.5 and 4.5 or 5. A TSH level of 10 mIU/L or higher is typically indicative of hypothyroidism. A TSH level of 4.5 to 10 mIU/L is considered indicative of subclinical hypothyroidism.

What causes high TSH levels? ›

Causes of High TSH
  • 1) Hypothyroidism (Underactive Thyroid) TSH often increases in response to an underactive thyroid gland (primary hypothyroidism) [1]. ...
  • 2) Iodine Deficiency or Excess. ...
  • 3) Obesity. ...
  • 4) Radiation Therapy. ...
  • 5) Pituitary Tumors. ...
  • 6) Some Toxins, Drugs, and Supplements. ...
  • 7) Rare Genetic Disorders. ...
  • 8) Aging.
Jan 19, 2021

What does it mean if your TSH is low but your T3 and T4 are normal? ›

If you had thyroid blood tests and the results indicate that your TSH levels are low or undetectable (0.1 to 0.4 mIU/L) and your thyroxine (T4) and triiodothyronine (T3) levels are in the normal range, it means you have subclinical hyperthyroidism.

How do you know if your TSH is high? ›

TSH is a hormone that is created by the pituitary gland that tells the thyroid gland how much thyroid hormone to make. Symptoms of high TSH include fatigue, depression, cold intolerance, constipation, infertility and other symptoms.

Why is TSH low in hyperthyroidism? ›

TSH prompts the thyroid to make more thyroid hormones in response to low levels. If the thyroid hormone levels are too high, referred to as hyperthyroidism or overactive thyroid, the pituitary will produce less TSH in an attempt to decrease production of active thyroid hormone.

What is alpha subunit of TSH? ›

Pituitary glycoprotein hormones FSH (follicle-stimulating hormone), LH (luteinizing hormone) and thyrotropic hormone, TSH (thyroid-stimulating hormone) are formed by two subunits: alpha which is essentially the same for all three hormones, and beta which is responsible for their biochemical specificity.

What is a subunit of FSH? ›

Follicle-stimulating hormone (FSH) comprises an alpha subunit and a beta subunit, whereas the FSH receptor consists of two halves with distinct functions: the N-terminal extracellular exodomain and C-terminal membrane-associated endodomain.

What effect does thyroid hormone have on beta receptors? ›

Our results indicate that thyroid hormone enhances the number of beta-adrenergic receptor binding sites by synthesizing new receptor proteins resulting in increased catecholamine sensitivity.


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