KP-10/Gpr54 attenuates rheumatic arthritis through inactivating NF-κB and MAPK signaling in macrophages.

Wang D, Wu Z, Zhao C, Yang X, Wei H, Liu M, Zhao J, Qian M, Li Z, Xiao J

Pharmacological research17 Feb 2021Cited by 30 (Europe PMC)

PMID33609696DOI10.1016/j.phrs.2021.105496PepBankPUB-33609696

Publisher page PubMedAsk about this study

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study7

5 results from studies that gave the peptide. No result from this study comes from people.

01AnimalAnimal study (in vivo)Efficacy outcome
In mice with collagen-induced arthritis, KP-10 ameliorated arthritis symptoms.
In plain wordsIn mice with arthritis, KP-10 eased arthritis symptoms.
Peptide
Kisspeptin-10
Outcome
DecreaseCIA symptoms
Study
mousen: not reported in source
Collagen-induced arthritis (CIA) mice
Outcome group
Bone and joint · Musculoskeletal
Studied dose
Dose not stated
Source sentences
Summary
while KP-10 reduced the LPS-induced inflammatory cytokines in vitro and ameliorated the CIA symptoms in vivo.
Report a problemFND-3360969602
02LabIn vitro (cells)Mechanism
In bone marrow-derived macrophages, KP-10 reduced the inflammatory cytokines induced by lipopolysaccharide.
In plain wordsIn cells, KP-10 reduced inflammatory signals caused by LPS.
Peptide
Kisspeptin-10
Outcome
DecreaseLPS-induced inflammatory cytokines
Study
n: not reported in source
LPS-stimulated bone marrow-derived macrophages (BMDM)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
while KP-10 reduced the LPS-induced inflammatory cytokines in vitro
Report a problemFND-3360969601
03LabIn vitro (cells)Mechanism
In bone marrow-derived macrophages, KP-10/GPR54 bound to PP2A-C.
In plain wordsIn cells, KP-10 and its receptor GPR54 bound to a protein called PP2A-C.
Peptide
Kisspeptin-10
Outcome
Not applicableKP-10/GPR54 binding to PP2A-C
Study
n: not reported in source
LPS-stimulated bone marrow-derived macrophages (BMDM)
Outcome group
Receptor activity and mechanism · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, we demonstrated that KP-10/GPR54 binds to PP2A-C to suppressed LPS induced NF-κB and MAPK signaling in BMDM.
Report a problemFND-3360969605
04LabIn vitro (cells)Mechanism
In bone marrow-derived macrophages, KP-10/GPR54 suppressed LPS-induced NF-kB signaling.
In plain wordsIn cells, KP-10 and its receptor reduced NF-kB inflammatory signaling caused by LPS.
Peptide
Kisspeptin-10
Outcome
DecreaseLPS-induced NF-kB signaling
Study
n: not reported in source
LPS-stimulated bone marrow-derived macrophages (BMDM)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, we demonstrated that KP-10/GPR54 binds to PP2A-C to suppressed LPS induced NF-κB and MAPK signaling in BMDM.
Report a problemFND-3360969606
05LabIn vitro (cells)Mechanism
In bone marrow-derived macrophages, KP-10/GPR54 suppressed LPS-induced MAPK signaling.
In plain wordsIn cells, KP-10 and its receptor reduced MAPK inflammatory signaling caused by LPS.
Peptide
Kisspeptin-10
Outcome
DecreaseLPS-induced MAPK signaling
Study
n: not reported in source
LPS-stimulated bone marrow-derived macrophages (BMDM)
Outcome group
Inflammation markers · Immune and inflammation
Studied dose
Dose not stated
Source sentences
Summary
Furthermore, we demonstrated that KP-10/GPR54 binds to PP2A-C to suppressed LPS induced NF-κB and MAPK signaling in BMDM.
Report a problemFND-3360969607

Studies that did not test the peptide alone2

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

06AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Mechanism
In collagen-induced arthritis mice, Gpr54 knockout increased disease severity.
In plain wordsIn mice, removing the KP-10 receptor Gpr54 made arthritis more severe.
Peptide
Kisspeptin-10
Outcome
IncreaseCIA severity in Gpr54 knockout
Study
mousen = 10
Collagen-induced arthritis (CIA) mice
Outcome group
Bone and joint · Musculoskeletal
Source sentences
Summary
In addition, Gpr54^-/- increased the inflammatory cytokines induced by lipopolysaccharide (LPS) in BMDM and diseased severity of CIA (n = 10), while KP-10 reduced the LPS-induced inflammatory cytokines in vitro and ameliorated the CIA symptoms in vivo.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-3360969604
07LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism
In bone marrow-derived macrophages, Gpr54 knockout increased LPS-induced inflammatory cytokines.
In plain wordsIn cells, removing the KP-10 receptor Gpr54 increased inflammatory signals caused by LPS.
Peptide
Kisspeptin-10
Outcome
IncreaseLPS-induced inflammatory cytokines in Gpr54 knockout
Study
n: not reported in source
Gpr54-knockout bone marrow-derived macrophages
Outcome group
Inflammation markers · Immune and inflammation
Source sentences
Summary
In addition, Gpr54^-/- increased the inflammatory cytokines induced by lipopolysaccharide (LPS) in BMDM and diseased severity of CIA (n = 10), while KP-10 reduced the LPS-induced inflammatory cytokines in vitro and ameliorated the CIA symptoms in vivo.
In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.
Report a problemFND-3360969603

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 09:43 UTC
Study results updated
Version 1
9 Oct 2026, 03:04 UTC
First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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