Evidence map›Paper›PMID 33212319›Full record

ArticleBone2021

Osteoblastic monocyte chemoattractant protein-1 (MCP-1) mediation of parathyroid hormone's anabolic actions in bone implicates TGF-β signaling.

Jawed A Siddiqui, Carole Le Henaff, Joshua Johnson, Zhiming He, Daniel B Rifkin, Nicola C Partridge

Open access · greenAbstract read
In one paragraph

Article in Bone, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed, 1 pooled it
0.6field-weighted citation impact, top 34% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Jawed A SiddiquiDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, United States of America.
Carole Le HenaffDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, United States of America.
Joshua JohnsonDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, United States of America.
Zhiming HeDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, United States of America.
Daniel B RifkinDepartment of Cell Biology, New York University Grossman School of Medicine, New York, United States of America.
Nicola C PartridgeDepartment of Molecular Pathobiology, New York University College of Dentistry, New York, United States of America. Electronic address: ncp234@nyu.edu.
New York University · US

Funding

Project-005UL1TR001445 · NCATS · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI BREDELLA, MIRIAM ANTOINETTE, HOCHMAN, JUDITH S · 2015 to 2025
$103.5M
Skyscan 1172 Ex-vivo MicroComputed Tomography SystemS10OD010751 · OD · NEW YORK UNIVERSITY · PI PARTRIDGE, NICOLA C · 2013 to 2013
$326k
NCATS NIH HHS UL1 TR001445NIH HHS S10 OD010751
6 · The paper itself

Abstract

Parathyroid hormone (PTH) is necessary for the regulation of calcium homeostasis and PTH (1-34) was the first approved osteoanabolic therapy for osteoporosis. It is well established that intermittent PTH increases bone formation and that bone remodeling and several cytokines and chemokines play an essential role in this process. Earlier, we had established that the chemokine, monocyte chemoattractant protein-1 (MCP-1/CCL2), was the most highly stimulated gene in rat bone after intermittent PTH injections. Nevertheless, MCP-1 function in bone appears to be complicated. To identify the primary cells expressing MCP-1 in response to PTH, we performed in situ hybridization of rat bone sections after hPTH (1-34) injections and showed that bone-lining osteoblasts are the primary cells that express MCP-1 after PTH treatment. We previously demonstrated MCP-1's importance by showing that PTH's anabolic effects are abolished in MCP-1 null mice, further implicating a role for the chemokine in this process. To establish whether rhMCP-1 peptide treatment could rescue the anabolic effect of PTH in MCP-1 null mice, we treated 4-month-old wild-type (WT) mice with hPTH (1-34) and MCP-1

Indexed as

Anabolic AgentsTransforming Growth Factor betaAnimalsBone and BonesChemokine CCL2MiceOsteoblastsParathyroid HormoneRatsX-Ray MicrotomographyAnabolic AgentsCcl2 protein, mouseChemokine CCL2Parathyroid HormoneTransforming Growth Factor betaBoneChemokinesMonocyte chemoattractant protein-1OsteoporosisPTH

Identifiers

PMID33212319
PMCPMC8628523
OpenAlexW3098851521

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.