PMID- 35417489
OWN - NLM
STAT- MEDLINE
DCOM- 20220415
LR  - 20220622
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 17
IP  - 4
DP  - 2022
TI  - Retinoid-X receptor agonists increase thyroid hormone competence in lower jaw 
      remodeling of pre-metamorphic Xenopus laevis tadpoles.
PG  - e0266946
LID - 10.1371/journal.pone.0266946 [doi]
LID - e0266946
AB  - Thyroid hormone (TH) signaling plays critical roles during vertebrate 
      development, including regulation of skeletal and cartilage growth. TH acts 
      through its receptors (TRs), nuclear hormone receptors (NRs) that heterodimerize 
      with Retinoid-X receptors (RXRs), to regulate gene expression. A defining 
      difference between NR signaling during development compared to in adult tissues, 
      is competence, the ability of the organism to respond to an endocrine signal. 
      Amphibian metamorphosis, especially in Xenopus laevis, the African clawed frog, 
      is a well-established in vivo model for studying the mechanisms of TH action 
      during development. Previously, we've used one-week post-fertilization X. laevis 
      tadpoles, which are only partially competent to TH, to show that in the tail, 
      which is naturally refractive to exogenous T3 at this stage, RXR agonists 
      increase TH competence, and that RXR antagonism inhibits the TH response. Here, 
      we focused on the jaw that undergoes dramatic TH-mediated remodeling during 
      metamorphosis in order to support new feeding and breathing styles. We used a 
      battery of approaches in one-week-old tadpoles, including quantitative 
      morphology, differential gene expression and whole mount cell proliferation 
      assays, to show that both pharmacologic (bexarotene) and environmental 
      (tributyltin) RXR agonists potentiated TH-induced responses but were inactive in 
      the absence of TH; and the RXR antagonist UVI 3003 inhibited TH action. Bex and 
      TBT significantly potentiated cellular proliferation and the TH induction of 
      runx2, a transcription factor critical for developing cartilage and bone. 
      Prominent targets of RXR-mediated TH potentiation were members of the matrix 
      metalloprotease family, suggesting that RXR potentiation may emphasize pathways 
      responsible for rapid changes during development.
FAU - Mengeling, Brenda J
AU  - Mengeling BJ
AUID- ORCID: 0000-0002-4681-7601
AD  - Department of Neurobiology, Physiology, and Behavior, College of Biological 
      Sciences, University of California, Davis, California, United States of America.
FAU - Vetter, Lara F
AU  - Vetter LF
AUID- ORCID: 0000-0002-1899-2672
AD  - Department of Neurobiology, Physiology, and Behavior, College of Biological 
      Sciences, University of California, Davis, California, United States of America.
FAU - Furlow, J David
AU  - Furlow JD
AD  - Department of Neurobiology, Physiology, and Behavior, College of Biological 
      Sciences, University of California, Davis, California, United States of America.
LA  - eng
GR  - P42 ES004699/ES/NIEHS NIH HHS/United States
GR  - R21 ES026271/ES/NIEHS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20220413
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Receptors, Thyroid Hormone)
RN  - 0 (Retinoid X Receptors)
RN  - 0 (Retinoids)
RN  - 0 (Thyroid Hormones)
SB  - IM
MH  - Animals
MH  - Gene Expression Regulation, Developmental
MH  - Larva
MH  - Metamorphosis, Biological/physiology
MH  - *Receptors, Thyroid Hormone/genetics/metabolism
MH  - Retinoid X Receptors/genetics
MH  - Retinoids/pharmacology
MH  - *Thyroid Hormones/metabolism
MH  - Xenopus laevis/genetics
PMC - PMC9007347
COIS- The authors have declared that no competing interests exist.
EDAT- 2022/04/14 06:00
MHDA- 2022/04/16 06:00
PMCR- 2022/04/13
CRDT- 2022/04/13 17:12
PHST- 2021/08/29 00:00 [received]
PHST- 2022/03/30 00:00 [accepted]
PHST- 2022/04/13 17:12 [entrez]
PHST- 2022/04/14 06:00 [pubmed]
PHST- 2022/04/16 06:00 [medline]
PHST- 2022/04/13 00:00 [pmc-release]
AID - PONE-D-21-28036 [pii]
AID - 10.1371/journal.pone.0266946 [doi]
PST - epublish
SO  - PLoS One. 2022 Apr 13;17(4):e0266946. doi: 10.1371/journal.pone.0266946. 
      eCollection 2022.