PIPages
Labs

Chia-Lung Wu

University of Rochester, NY·Biomedical Engineering

Hip osteoarthritis (OA), the painful wearing-down of joint cartilage, affects one in four people by age 85, and no drugs yet slow the disease. It is linked to abnormal hip shape, including cam-type femoroacetabular impingement (FAI), where bone rubs inside the joint.

Fields

Biomedical Engineering

Medicine & Clinical Research

Biology

Topics

osteoarthritis

femoroacetabular impingement

cartilage

Grants
1 known grant, through Aug 2029

What they work on

  1. Determine how mechanical loading switches on WNT16 in chondrocytes through the force-sensing calcium channel TRPV4, by loading human stem cell-derived and hip chondrocytes in agarose gels and sequencing their genetic and epigenetic controls.
  2. Test whether mice lacking Wnt16 in cartilage develop worse hip OA, measuring cartilage damage, joint inflammation, bone remodeling, behavior and pain, and test WNT16 effects on hypertrophy in human hip chondrocytes.
  3. Map chondrocyte types and cell-to-cell signaling in healthy, FAI and OA hip cartilage using single-cell and spatial RNA sequencing, and test whether nanoparticle delivery of WNT16 mRNA slows OA in cartilage explants.

More about the research

Studying FAI hips can therefore reveal what drives early OA. The team compared FAI and OA cartilage with RNA sequencing. They found that levels of WNT16, a signaling protein, fall as OA becomes more severe. WNT16 also drops as chondrocytes, the cells that build cartilage, enlarge in a process called hypertrophy, a hallmark of OA. It rises when chondrocytes are mechanically loaded. This points to a link with TRPV4, a calcium channel through which chondrocytes sense mechanical force.

Why it matters

Hip osteoarthritis is a painful, common joint disease with no disease-modifying drugs and a heavy healthcare burden. By clarifying how WNT16 protects hip cartilage, this work could point to early treatments for people with hip OA or FAI, such as delivering WNT16 mRNA with nanoparticles to restore protective signaling.

Known grants

From NIH and NSF research grants. Labs often have other funding we can't see.

WNT signaling in chondrocyte biology and osteoarthritis

NIH · Sep 2024 – Aug 2029

Closest labs

X. Lucas Lu

University of Delaware, DE·Biomedical Engineering

Determine whether statin use is linked to lower rates of osteoarthritis in the Delaware population, using a retrospective cohort study of existing health records.

David Reed

University of Illinois Chicago, IL·Biology

Test whether injury-induced loss of Collagen VI drives cartilage degeneration in a surgically induced mouse model of TMJ osteoarthritis.

Sanja Novak

University of Arkansas for Medical Sciences, AR·Physiology

Evaluate how blood vessels in the synovium and subchondral bone change during OA development. Test whether early microvascular damage or later synovial angiogenesis drives cartilage damage, including after mechanical-stress knee injury.

The school

University of Rochester: 38 labs on PI Pages, $492M a year on research, 308 research doctorates a year.

More about University of Rochester

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