Related Experiment Video

Updated: Jun 29, 2025

Non-invasive In Vivo Fluorescence Optical Imaging of Inflammatory MMP Activity Using an Activatable Fluorescent Imaging Agent
06:46

Non-invasive In Vivo Fluorescence Optical Imaging of Inflammatory MMP Activity Using an Activatable Fluorescent Imaging Agent

Published on: May 8, 2017

8.8K

PIM Kinases as Potential Biomarkers and Therapeutic Targets in Inflammatory Arthritides

Elisa Assirelli1, Jacopo Ciaffi1, Valentina Scorcu1

  • 1Medicine and Rheumatology Unit, IRCCS Istituto Ortopedico Rizzoli, 40136 Bologna, Italy.

International Journal of Molecular Sciences
|March 28, 2024
PubMed

Insights

PIM kinases are deregulated in inflammatory arthritis, with altered PIM-1 and PIM-3 protein levels observed in patients with rheumatoid arthritis, psoriatic arthritis, and axial spondyloarthritis compared to healthy individuals. Treatment did not alter these PIM kinase levels.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • PIM kinases (PIM-1, -2, -3) regulate key cellular processes like survival and proliferation.
  • PIM kinases are implicated in rheumatoid arthritis pathogenesis.
  • Their role in psoriatic arthritis and axial spondyloarthritis remains unexplored.

Purpose of the Study:

  • To investigate PIM kinase expression in inflammatory arthritides (RA, PsA, axSpA).
  • To correlate PIM kinase levels with pro-inflammatory cytokines.
  • To assess changes in PIM kinase expression following treatment with biologic DMARDs or JAK inhibitors.

Main Methods:

  • Gene and protein expression analysis of PIM-1, -2, and -3.
  • Samples included peripheral blood mononuclear cells and serum from RA, PsA, axSpA patients, and healthy controls.
  • Expression levels were compared between groups and after 6 months of therapy.

Main Results:

  • PIM-1, -2, and -3 kinases were expressed at both gene and protein levels in all samples.
  • PIM-1 protein was highest, PIM-3 lowest.
  • Patients showed reduced PIM-1 and increased PIM-3 protein compared to controls, with no differences between disease types.
  • Therapy did not alter PIM kinase levels.

Conclusions:

  • Preliminary data suggest PIM pathway deregulation in inflammatory arthritides.
  • Further research is needed to elucidate the specific role of PIM kinases in these conditions.
  • PIM kinases represent a potential therapeutic target in inflammatory arthritis.
Keywords:
PIM kinasesaxial spondyloarthritispsoriatic arthritisrheumatoid arthritis

More Related Videos

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

95
Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response12:50

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

6.6K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
8.9K
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
5.5K
Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists01:23

Treatment for Pulmonary Arterial Hypertension: Prostacyclin Receptor Agonists

Prostacyclin receptor agonists are a class of therapeutic agents integral to managing pulmonary arterial hypertension (PAH). These drugs operate by mimicking the action of prostaglandin I2, or PGI2, a naturally occurring compound in the body.
These agonists bind to the IPR receptor situated on the plasma membrane of the pulmonary artery smooth muscle cells. This binding triggers a cascade of reactions known as the GS-AC-cAMP-PKA pathway. This pathway results in the relaxation of smooth muscle...
173
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include:
2.5K
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
8.5K