Environmental Manipulations as an Effective Alternative Treatment to Reduce Endometriosis Progression

Torres-Reverón, Annelyn; Rivera, Leslie L.; Flores, Idhaliz; Appleyard, Caroline B.

doi:10.1177/1933719117741374

Cited by 12 publications

(22 citation statements)

References 67 publications

(95 reference statements)

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“…Surgical induction of endometriosis followed the protocol previously published [ 31 , 32 , 33 ]. Briefly, rats were anesthetized with isoflurane and four pieces of the right uterine horn were auto transplanted to 4 different blood vessels in the intestinal mesentery.…”

Section: Methodsmentioning

confidence: 99%

“…For experiment 1, sham or endometriosis operated rats were allowed to progress for 7 days after surgery. For experiment 2, endometriosis was allowed to progress for 60 days before sacrificing, similar to our previous report [ 32 , 33 ].…”

Section: Methodsmentioning

confidence: 99%

“…At the end of the testing period, animals were returned to the home cage and after a 5-min break were tested in the elevated zero-maze. For easier comparison purposes with the zero maze (described below) and our previous publication [ 33 ], we analyzed and graphed the first 5 minutes of the open field test.…”

Section: Methodsmentioning

confidence: 99%

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Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

et al. 2018

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Endometriosis is a disorder in which endometrial tissue is found outside the uterus causing pain, infertility and stress. Finding effective, non-hormonal and long-term treatments for endometriosis still remains one of the most significant challenges in the field. Corticotropin releasing hormone (CRH) is one of the main signaling peptides within the hypothalamic pituitary adrenal (HPA) axis released in response to stress. CRH can affect nervous and visceral tissues such as the uterus and gut via activation of two types of CRH receptors: CRHR1 and CRHR2. Our aim was to determine if blocking CRHR1 with antalarmin will reduce endometriosis progression. In experiment 1 we induced endometriosis in female rats by suturing uterine horn tissue next to the intestinal mesentery and allowed to progress for 7 days. We determined that after 7 days, there was a significant increase in CRHR1 within endometriotic vesicles as compared to normal uterus. In Experiment 2, we induced endometriosis and administered either antalarmin (20 mg/kg, i.p.) or vehicle during the first 7 days after surgery. A separate group of sham surgery rats served as non-endometriosis controls. Endometriosis was allowed to progress until 60 days after surgery, at which time rats were tested for anxiety behaviors. At the time of sacrifice, endometriotic vesicles, uterus and blood were collected. Treatment with antalarmin significantly reduced the size (67% decrease) and number (30% decrease) of endometriotic vesicles. Antalarmin also prevented the increase in CRH and CRHR1 mRNA within endometriotic vesicles but not of glucocorticoid receptor. Endometriosis did not change anxiety behaviors in the open field and zero-maze tests and prior antalarmin administration did not modify this. Our data provides the first in-vivo demonstration for use of CRHR1 antagonist for the treatment of endometriosis opening the possibility for further exploring CRH signaling as a treatment target for this debilitating disease.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

et al. 2018

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“…Therefore, an up regulation of CRHR1 signaling within the adrenals might be a compensatory mechanism in response to prior antalarmin administration that is being partially counterbalanced by CRHR2 mRNA increase in order to regulate catecholamine secretion after antalarmin administration (Fig 5). In this, and both of our previous studies [22,27], sham operated animals served as the controls against which mRNA expression was normalized to measure the effects in rats with endometriosis. Since surgical interventions per se pose as a physiological stressor to the animal, comparing against sham groups is an important factor.…”

Section: Discussionmentioning

confidence: 99%

Short treatment with antalarmin alters adrenal gland receptors in the rat model of endometriosis

et al. 2020

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Endometriosis is a chronic inflammatory disorder in which endometrial tissue is found outside the uterine cavity. Previous reports suggest that there is a dysregulation of the hypothalamic pituitary adrenal axis during the progression of endometriosis. Our previous report showed that a short-term treatment with antalarmin, a corticotrophin releasing hormone receptor type 1 (CRHR1) antagonist decreases the number and size of endometriotic vesicles in the auto-transplantation rat model of endometriosis. Our current goal was to examine the mRNA expression of intra-adrenal receptors to better understand the mechanisms of the hypothalamic pituitary adrenal (HPA) axis involvement in endometriosis. We used two groups of female rats. The first received sham surgery or endometriosis surgery before collecting the adrenals after 7 days of the disease progression. The second group of animals received endometriosis surgery and a treatment of either vehicle or antalarmin (20 mg/kg, i. p.) during the first 7 days after endometriosis induction and then the disease was allowed to progress until day 60. Rats with sham surgery served as controls. Results showed that the mRNA expression of the mineralocorticoid (MRC2) receptor was lower in the rats after 7 days of endometriosis surgery and in rats with endometriosis that received antalarmin. In addition, the CRHR1 was significantly elevated in animals that received antalarmin and this was counteracted by a non-significant elevation in CRHR2 mRNA. The glucocorticoid receptor mRNA within the adrenals was not affected by endometriosis or antalarmin treatment. This report is one of the first to explore intra-adrenal mRNA for receptors involved in the HPA axis signaling as well as in the sympatho-adrenal signaling, calling for additional research towards understanding the role of the adrenal glands in chronic inflammatory diseases such as endometriosis.

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“…For group 1, sham or endometriosis operated rats were allowed to progress for 7 days after surgery. For group 2, endometriosis was allowed to progress for 60 days before sacrificing, similar to our previous report (31;30).…”

Section: Methodsmentioning

confidence: 99%

Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

Torres-Reverón

Rivera-Lopez

Flores

et al. 2018

Preprint

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Endometriosis is a disorder in which endometrial tissue is found outside the uterus causing pain, infertility and stress. Finding an effective and long-term treatment for endometriosis still remains one of the most significant challenges in the field. Corticotropin releasing hormone (CRH) is one of the main signaling peptides within the hypothalamic pituitary adrenal (HPA) axis released in response to stress. CRH can affect nervous and visceral tissues such as the uterus and gut via activation of two types of CRH receptors: CRHR1 and CRHR2. Our aim was to determine if blocking CRHR1 with antalarmin will reduce endometriosis progression. First, we induced endometriosis in female rats by suturing uterine horn tissue next to the intestinal mesentery and allowed to progress for 7 days. We determined that after 7 days, there was a significant increase in CRHR1 within endometriotic vesicles as compared to normal uterus. A second group of rats received endometriosis but also antalarmin (20 mg/kg, i.p.) during the first 7 days after surgery. As separate group of sham surgery rats served as controls. Endometriosis was allowed to progress until 60 days after surgery. At time of sacrifice, rats were tested for anxiety behaviors and endometriotic vesicles, and uterus were collected. Rats with endometriosis that received antalarmin significantly reduced the size (67% decrease) and number (30% decrease) of endometriotic vesicles. Antalarmin also prevented the increase in CRH and CRHR1 within endometriotic vesicles but not of glucocorticoid receptor. Behaviorally, endometriosis increased anxiety in the zero-maze test but antalarmin did not modify it. Our data provides the first demonstration for the effective use on CRHR1 antagonist for the treatment of endometriosis with promising effects for long-term therapy of this debilitating disease.

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Environmental Manipulations as an Effective Alternative Treatment to Reduce Endometriosis Progression

Cited by 12 publications

References 67 publications

Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

Short treatment with antalarmin alters adrenal gland receptors in the rat model of endometriosis

Antagonizing the corticotropin releasing hormone receptor 1 with antalarmin reduces the progression of endometriosis

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