The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice

Neeraja Purandare; Nardhy Gomez-Lopez; Marcia Arenas-Hernandez; Jose Galaz; Roberto Romero; Yue Xi; Andrew M. Fribley; Lawrence I. Grossman; Siddhesh Aras

doi:10.1016/j.placenta.2023.07.005

The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice

Neeraja Purandare, Nardhy Gomez-Lopez, Marcia Arenas-Hernandez, Jose Galaz, Roberto Romero, Yue Xi, Andrew M. Fribley, Lawrence I. Grossman, Siddhesh Aras

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that genetic and pharmacological increases in MNRR1 levels can counter the inflammatory profile. Herein, we show that nitazoxanide, a clinically approved drug, is an activator of MNRR1 and abrogates preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection.

Original language	English
Pages (from-to)	66-71
Number of pages	6
Journal	Placenta
Volume	140
DOIs	https://doi.org/10.1016/j.placenta.2023.07.005
State	Published - Sep 7 2023

Keywords

CHCHD2
Decidua
Intra-amniotic infection
Intra-amniotic inflammation
Nitazoxanide (Alinia)
Prematurity
Preterm labor

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10.1016/j.placenta.2023.07.005

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title = "The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice",

abstract = "Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that genetic and pharmacological increases in MNRR1 levels can counter the inflammatory profile. Herein, we show that nitazoxanide, a clinically approved drug, is an activator of MNRR1 and abrogates preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection.",

keywords = "CHCHD2, Decidua, Intra-amniotic infection, Intra-amniotic inflammation, Nitazoxanide (Alinia), Prematurity, Preterm labor",

author = "Neeraja Purandare and Nardhy Gomez-Lopez and Marcia Arenas-Hernandez and Jose Galaz and Roberto Romero and Yue Xi and Fribley, {Andrew M.} and Grossman, {Lawrence I.} and Siddhesh Aras",

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T1 - The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice

AU - Purandare, Neeraja

AU - Gomez-Lopez, Nardhy

AU - Arenas-Hernandez, Marcia

AU - Galaz, Jose

AU - Romero, Roberto

AU - Xi, Yue

AU - Fribley, Andrew M.

AU - Grossman, Lawrence I.

AU - Aras, Siddhesh

PY - 2023/9/7

Y1 - 2023/9/7

N2 - Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that genetic and pharmacological increases in MNRR1 levels can counter the inflammatory profile. Herein, we show that nitazoxanide, a clinically approved drug, is an activator of MNRR1 and abrogates preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection.

AB - Intra-amniotic inflammation leading to preterm birth is one of the leading causes of neonatal morbidity and mortality. We recently reported that the mitochondrial levels of MNRR1 (Mitochondrial Nuclear Retrograde, Regulator 1; also called CHCHD2, AAG10, or PARK22), an important bi-organellar regulator of cellular function, are reduced in the context of inflammation and that genetic and pharmacological increases in MNRR1 levels can counter the inflammatory profile. Herein, we show that nitazoxanide, a clinically approved drug, is an activator of MNRR1 and abrogates preterm birth in a well-characterized murine model caused by intra-amniotic lipopolysaccharide (LPS) injection.

KW - CHCHD2

KW - Decidua

KW - Intra-amniotic infection

KW - Intra-amniotic inflammation

KW - Nitazoxanide (Alinia)

KW - Prematurity

KW - Preterm labor

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DO - 10.1016/j.placenta.2023.07.005

M3 - Article

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AN - SCOPUS:85166655022

SN - 0143-4004

VL - 140

SP - 66

EP - 71

JO - Placenta

JF - Placenta

ER -

The MNRR1 activator nitazoxanide abrogates lipopolysaccharide-induced preterm birth in mice

Abstract

Keywords

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