Aim: To investigate the silencing effects of pAd-shRNA-pleiotrophin (PTN) on PTN in pancreatic cancer cells, and to observe the inhibition of pAd-shRNA-PTN on neurite outgrowth from dorsal root ganglion (DRG) neurons in vitro.
Methods: PAd-shRNA-PTN was used to infect pancreatic cancer BxPC-3 cells; assays were conducted for knockdown of the PTN gene on the 0th, 1st, 3rd, 5th, 7th and 9th d after infection using immunocytochemistry, real-time quantitative polymerase chain reaction (PCR), and Western blotting analysis. The morphologic changes of cultured DRG neurons were observed by mono-culture of DRG neurons and co-culture with BXPC-3 cells in vitro.
Results: The real-time quantitative PCR showed that the inhibition rates of PTN mRNA expression in the BxPC-3 cells were 20%, 80%, 50% and 25% on the 1st, 3rd, 5th and 7th d after infection. Immunocytochemistry and Western blotting analysis also revealed the same tendency. In contrast to the control, the DRG neurons co-cultured with the infected BxPC-3 cells shrunk; the number and length of neurites were significantly decreased.
Conclusion: Efficient and specific knockdown of PTN in pancreatic cancer cells and the reduction in PTN expression resulted in the inhibition of neurite outgrowth from DRG neurons.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3110932 | PMC |
| http://dx.doi.org/10.3748/wjg.v17.i21.2667 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cycloastragenol promotes dorsal column axon regeneration in mice.
Front Cell Neurosci
January 2025
Key Laboratory of Novel Targets and Drug Study for Neural Repair of Zhejiang Province, School of Medicine, Hangzhou City University, Hangzhou, China.
Introduction: Cycloastragenol (CAG) has a wide range of pharmacological effects, including anti-inflammatory, antiaging, antioxidative, and antitumorigenic properties. In addition, our previous study showed that CAG administration can promote axonal regeneration in peripheral neurons. However, whether CAG can activate axon regeneration central nervous system (CNS) remains unknown.
View Article and Find Full Text PDFAging negatively impacts central nervous system function; however, the cellular impact of aging in the peripheral nervous system remains poorly understood. Aged individuals are more likely to experience increased pain and slower recovery after trauma. Such injury can damage vulnerable peripheral axons of dorsal root ganglion (DRG) neurons resulting in somatosensory dysfunction.
View Article and Find Full Text PDFMETTL14-mediated m6A modification of TRPA1 promotes acute visceral pain induced by uterine cervical dilation by promoting NR2B phosphorylation.
Cell Signal
January 2025
Department of Anesthesia, Jiaxing University Affiliated Women and Children Hospital, Jiaxing 314050, Zhejiang Province, PR China. Electronic address:
Background: While TRPA1 serves as a therapeutic target for nociceptive pain, its role in acute visceral pain induced by uterine cervical dilation (UCD) remains an enigma. This study aims to elucidate the upstream and downstream mechanisms of TRPA1 in the context of UCD-induced acute visceral pain.
Methods: The UCD rats were administered with SAH (inhibitor of the METTL3-METTL14 complex) via intrathecal tubing.
Histone Methyltransferase G9a in Primary Sensory Neurons Promotes Inflammatory Pain and Transcription of and via Bivalent Histone Modifications.
J Neurosci
January 2025
Center for Neuroscience and Pain Research, Department of Anesthesiology and Perioperative Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA
Transient receptor potential ankyrin 1 (TRPA1) and vanilloid 1 (TRPV1) channels are crucial for detecting and transmitting nociceptive stimuli. Inflammatory pain is associated with sustained increases in TRPA1 and TRPV1 expression in primary sensory neurons. However, the epigenetic mechanisms driving this upregulation remain unknown.
View Article and Find Full Text PDFAction potential-independent spontaneous microdomain Ca transients-mediated continuous neurotransmission regulates hyperalgesia.
Proc Natl Acad Sci U S A
January 2025
Department of Neurology, the Second Affiliated Hospital, Neuroscience Research Center, Key Laboratory of Biomedical Information Engineering of Ministry of Education, School of Life Science and Technology, Xi'an Jiaotong University, Xi'an 710000, China.
Neurotransmitters and neuromodulators can be released via either action potential (AP)-evoked transient or AP-independent continuous neurotransmission. The elevated AP-evoked neurotransmission in the primary sensory neurons plays crucial roles in hyperalgesia. However, whether and how the AP-independent continuous neurotransmission contributes to hyperalgesia remains largely unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!