Last update 01 Nov 2024

OSR1

Last update 01 Nov 2024

Basic Info

Synonyms

ODD, odd-skipped related transcription factor 1, OSR1

+ [1]

Introduction

Transcription factor that plays a role in the regulation of embryonic heart and urogenital development.

Drugs associated with OSR1

Rafoxanide

Target

OSR1 x STK39

Mechanism

OSR1 inhibitors [+1]

Active Org.

University of Birmingham

Originator Org.

University of Birmingham

Active Indication

Hypertension

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

closantel

Target

OSR1 x STK39

Mechanism

OSR1 inhibitors [+1]

Active Org.

University of Birmingham

Originator Org.

University of Birmingham

Active Indication

Hypertension

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with OSR1

100 Translational Medicine associated with OSR1

0 Patents (Medical) associated with OSR1

391

Literatures (Medical) associated with OSR1

01 Jan 2025·Developmental Biology

Drivers of vessel progenitor fate define intermediate mesoderm dimensions by inhibiting kidney progenitor specification

Article

Author: Perens, Elliot A. ; Yelon, Deborah ; Perens, Elliot A

Proper organ formation depends on the precise delineation of organ territories containing defined numbers of progenitor cells. Kidney progenitors reside in bilateral stripes of posterior mesoderm that are referred to as the intermediate mesoderm (IM). Previously, we showed that the transcription factors Hand2 and Osr1 act to strike a balance between the specification of the kidney progenitors in the IM and the vessel progenitors in the laterally adjacent territory. Recently, the transcription factor Npas4l - an early and essential driver of vessel and blood progenitor formation - was shown to inhibit kidney development. Here we demonstrate how kidney progenitor specification is coordinated by hand2, osr1, and npas4l. We find that npas4l and the IM marker pax2a are transiently co-expressed in the posterior lateral mesoderm, and npas4l is necessary to inhibit IM formation. Consistent with the expression of npas4l flanking the medial and lateral sides of the IM, our findings suggest roles for npas4l in defining the IM boundaries at each of these borders. At the lateral IM border, hand2 promotes and osr1 inhibits the formation of npas4l-expressing lateral vessel progenitors, and hand2 requires npas4l to inhibit IM formation and to promote vessel formation. Meanwhile, npas4l appears to have an additional role in suppressing IM fate at the medial border: npas4l loss-of-function enhances hand2 mutant IM defects and results in excess IM generated outside of the lateral hand2-expressing territory. Together, our findings reveal that establishment of the medial and lateral boundaries of the IM requires inhibition of kidney progenitor specification by the neighboring drivers of vessel progenitor fate.

01 Sep 2024·Molecular Therapy

Osr1-mediated mesothelial transition of liver mesenchymal cells exacerbates fibrotic liver damage

Article

Author: Lin, Pengyan ; Zhou, Bin ; Gao, Jie ; Yu, Donglin ; Nian, Xinxin ; Zhao, Yang ; Yang, Xinyan ; Bai, Yunfei

In chronic liver diseases, hepatic stellate cells (HSCs) are induced to form the myofibroblasts responsible for scar formation, leading to liver fibrosis and cirrhosis. Here, single-cell RNA sequencing with in vivo lineage tracing in nonalcoholic steatohepatitis (NASH) model mice reveals a subpopulation of HSCs transitioning back to a state resembling their developmental precursors, mesothelial cells (MCs), after liver injury. These damage-associated intermediates between HSCs and MCs (DIHMs) can be traced with a dual recombinase system by labeling Krt19-expressing cells within prelabeled Pdgfrb⁺ HSCs, and DIHMs highly express inflammation- and fibrosis-associated genes. Cre and Dre-inducible depletion of DIHMs by administering diphtheria toxin reduces liver fibrosis and alleviates liver damage in NASH model mice. Importantly, knockdown of Osr1, a zinc finger transcription factor of the OSR gene family, can block DIHM induction in vitro. Conditional knockout Osr1 in Pdgfrb-expressing mesenchymal cells in NASH model mice can reduce liver fibrosis in vivo. Our study collectively uncovers an injury-induced developmental reversion process wherein HSCs undergo what we call a mesenchymal-to-mesothelial transition, which can be targeted to develop interventions to treat chronic liver diseases.

01 Sep 2024·Development

Mesenchymal Osr1+ cells regulate embryonic lymphatic vessel formation

Article

Author: Kühnlein, Mira Nicola ; Giesecke-Thiel, Claudia ; Kotsaris, Georgios ; Vallecillo-García, Pedro ; Hägerling, René ; Orgeur, Mickael ; Hansmeier, Nils Rouven ; Meisen, Zarah Gertrud ; Timmermann, Bernd ; Stricker, Sigmar

ABSTRACTThe lymphatic system is formed during embryonic development by the commitment of specialized lymphatic endothelial cells (LECs) and their subsequent assembly in primary lymphatic vessels. Although lymphatic cells are in continuous contact with mesenchymal cells during development and in adult tissues, the role of mesenchymal cells in lymphatic vasculature development remains poorly characterized. Here, we show that a subpopulation of mesenchymal cells expressing the transcription factor Osr1 are in close association with migrating LECs and established lymphatic vessels in mice. Lineage tracing experiments revealed that Osr1+ cells precede LEC arrival during lymphatic vasculature assembly in the back of the embryo. Using Osr1-deficient embryos and functional in vitro assays, we show that Osr1 acts in a non-cell-autonomous manner controlling proliferation and early migration of LECs to peripheral tissues. Thereby, mesenchymal Osr1+ cells control, in a bimodal manner, the production of extracellular matrix scaffold components and signal ligands crucial for lymphatic vessel formation.

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OSR1

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