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Translaminar Autonomous System Model for the Modulation of Intraocular and Intracranial Pressure in Human Donor Posterior Segments
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TIPARP is involved in the regulation of intraocular pressure

Youjia Zhang1,2, Maomao Song1,2, Yingwen Bi3

  • 1Department of Ophthalmology & Visual Science, Eye & ENT Hospital, Shanghai Medical College, Fudan University, Shanghai, 200031, China.

Communications Biology
|December 19, 2022
PubMed

Insights

Elevated intraocular pressure (IOP), a glaucoma risk factor, is linked to TIPARP. Inhibiting TIPARP in human trabecular meshwork cells altered extracellular matrix and cytoskeleton proteins, suggesting TIPARP as a therapeutic target.

Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Cell Biology

Background:

  • Elevated intraocular pressure (IOP) is the primary risk factor for glaucoma, but its molecular mechanisms remain poorly understood, hindering effective therapies.
  • 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-inducible Poly-ADP-ribose Polymerase (TIPARP) is a PARP family member involved in mono-ADP-ribosylation.

Purpose of the Study:

  • To investigate the role of TIPARP in the molecular mechanisms of elevated IOP and its potential as a therapeutic target for glaucoma.
  • To examine TIPARP expression in human ocular tissues and its association with primary open-angle glaucoma.

Main Methods:

  • Western blot and transcriptome analysis were used to assess TIPARP expression and its downstream effects on extracellular matrix and cytoskeleton proteins in human trabecular meshwork (HTM) cells.
  • TIPARP expression levels were analyzed in ocular tissues and blood from glaucoma patients and healthy controls.
  • The effect of a TIPARP inhibitor (RBN-2397) on IOP was evaluated in a rat model.

Main Results:

  • TIPARP was expressed in various human eye tissues and significantly upregulated in the blood and trabecular meshwork of primary open-angle glaucoma patients.
  • Downregulation or inhibition of TIPARP in HTM cells led to decreased expression of genes related to extracellular matrix deposition and cell adhesion, and increased levels of collagen, fibronectin, and α-SMA.
  • TIPARP inhibition also resulted in the production of cross-linked actin networks and upregulation of vinculin in HTM cells.
  • Subconjunctival injection of the TIPARP inhibitor RBN-2397 increased IOP in rats.

Conclusions:

  • TIPARP acts as a regulator of IOP by modulating extracellular matrix and cell cytoskeleton proteins within HTM cells.
  • These findings identify TIPARP as a promising therapeutic target for managing ocular hypertension and glaucoma.

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