Evidence map›Paper›PMID 24698731›Full record

ArticleExperimental cell research2014

Osteoblastic protein tyrosine phosphatases inhibition and connexin 43 phosphorylation by alendronate.

V Lezcano, T Bellido, L I Plotkin, R Boland, S Morelli

Open access · bronzeAbstract read
In one paragraph

Article in Experimental cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

9 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Protein⁻Protein Interactions with Connexin 43: Regulation and Function.International journal of molecular sciences · 2018
    Review
  7. Article
  8. Article
  9. Role of apoptosis in pathogenesis and treatment of bone-related diseases.Journal of orthopaedic surgery and research · 2015
    Review
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

5 authors at 3 institutions in 2 countries.

V LezcanoDepartamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, Bahía Blanca, Argentina.
T BellidoDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA; Department of Medicine, Division of Endocrinology, Indiana University, Indianapolis, IN, USA.
L I PlotkinDepartment of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, IN, USA.
R BolandDepartamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, Bahía Blanca, Argentina.
S MorelliDepartamento de Biología, Bioquímica y Farmacia, Universidad Nacional del Sur, Bahía Blanca, Argentina. Electronic address: smorelli@criba.edu.ar.
Universidad Nacional del Sur · ARIndiana University – Purdue University Indianapolis · USIndiana University School of Medicine

Funding

Glucocorticoid-induced Atrophy in Bone and MuscleR01AR059357 · NIAMS · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M. · 2011 to 2022
$3.4M
Bisphosphonate binding to connexin43-expressing cellsR03TW006919 · FIC · UNIV OF ARKANSAS FOR MED SCIS · PI BELLIDO, TERESITA M · 2005 to 2007
$101k
BLRD VA IK6 BX004596FIC NIH HHS R03 TW006919FIC NIH HHS R03TW006919NIAMS NIH HHS R01 AR059357
6 · The paper itself

Abstract

Bisphosphonates (BPs), potent inhibitors of bone resorption which inhibit osteoclasts, have also been shown to act on osteocytes and osteoblasts preventing apoptosis via connexin (Cx) 43 hemichannels and activating the extracellular signal regulated kinases ERKs. We previously demonstrated the presence of a saturable, specific and high affinity binding site for alendronate (ALN) in osteoblastic cells which express Cx43. However, cells lacking Cx43 also bound BPs. Herein we show that bound [(3)H]-alendronate is displaced by phosphatase substrates. Moreover, similar to Na3VO4, ALN inhibited the activity of transmembrane and cytoplasmic PTPs, pointing out the catalytic domain of phosphatases as a putative BP target. In addition, anti-phospho-tyrosine immunoblot analysis revealed that ALN stimulates tyrosine phosphorylation of several proteins of whole cell lysates, among which the major targets of the BP could be immunochemically identified as Cx43. Additionally, the transmembrane receptor-like PTPs, RPTPµ and RPTPα, as well as the cytoplasmic PTP1B, are highly expressed in ROS 17/2.8 cells. Furthermore, we evidenced that Cx43 interacts with RPTPµ in ROS 17/2.8 and ALN decreases their association. These results support the hypothesis that BPs bind and inhibit PTPs associated to Cx43 or not, which would lead to the activation of signaling pathways in osteoblasts.

Indexed as

AlendronateAnimalsBone Density Conservation AgentsCells, CulturedConnexin 43Enzyme InhibitorsHeLa CellsHumansOsteoblastsPhosphorylationProtein KinasesProtein Tyrosine PhosphatasesRatsAlendronateBone Density Conservation AgentsConnexin 43Enzyme InhibitorsGja1 protein, ratProtein KinasesProtein Tyrosine PhosphatasesAlendronateCx43 hemichannelsOsteoblastsProtein tyrosine phosphatases

Identifiers

PMID24698731
PMCPMC4076801
OpenAlexW2056853243

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.