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Updated: Jul 17, 2025
Isolation, Propagation, and Prion Protein Expression During Neuronal Differentiation of Human Dental Pulp Stem Cells
Published on: March 18, 2019
Investigating In Situ Expression of Neurotrophic Factors and Partner Proteins in Irreversible Pulpitis
Fatima Israr1, Syed Masood Ul Hasan1, Mushtaq Hussain2
1Dr Ishrat ul Ebad Khan Institute of Oral Health Sciences, Dow University of Health Sciences, Karachi, Pakistan; Bioinformatics and Molecular Medicine Research Group, Dow Research Institute of Biotechnology and Biomedical Sciences, Dow College of Biotechnology, Dow University of Health Sciences, Karachi, Pakistan.
Introduction:
In situ assessments of neurotrophic factors and their associated molecular partners have not been explored to date, particularly in humans. The present investigation aimed to explore the expressional dysregulation of neurotrophic factors (nerve growth factor [NGF], brain derived neurotrophic factor [BDNF], and NT4/5), their receptors (TrkA and TrkB), and their modulators (USP36 and Nedd4-2) directly in irreversibly inflamed human pulp tissues.
Methods:
Forty samples each of healthy and irreversibly inflamed pulp were extirpated for the study. Immunohistochemical examinations were carried out for the anatomic changes and expression of neurotrophic factors and partner proteins. Expression was digitally quantified using the IHC profiler module of ImageJ and deduced as optical density. Statistical analyses were carried out by GraphPad Prism.
Results:
Decrease in nuclear and vessel diameters was observed in irreversibly inflamed pulp tissues. NGF and BDNF were found to be significantly upregulated in symptomatic irreversible pulpitis (SIP), whereas no significant difference was observed in the expression of TrkA and TrkB. Expression of Nedd4-2, USP36, and TrkA was found positively correlated with the NGF in healthy pulp tissues. However, in SIP, positive correlation was only observed between the expression of USP36 and NGF. Among the ligands, BDNF expression was found positively correlated with NGF in healthy pulp but not with NT4/5. In the case of SIP, no correlation was observed between any neurotrophic factors.
Conclusions:
Upregulation of NGF, BDNF, USP36 and Nedd4-2 in SIP indicates dysregulation in the molecular events underlying the disease biology and could be exploited as potential markers for the disease diagnosis.
