tretinoin and Fish-Diseases

tretinoin has been researched along with Fish-Diseases* in 2 studies

Other Studies

2 other study(ies) available for tretinoin and Fish-Diseases

Article	Year
The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid-Inducible Gene-I-like Receptor Pathways. Journal of immunology (Baltimore, Md. : 1950), 2022, 07-15, Volume: 209, Issue:2 Nervous necrosis virus (NNV), a highly pathogenic RNA virus, is a major pathogen in the global aquaculture industry. To efficiently infect fish, NNV must evade or subvert the host IFN for their replication; however, the precise mechanisms remain to be elucidated. In this study, we reported that capsid protein (CP) of red-spotted grouper NNV (RGNNV) suppressed the IFN antiviral response to promote RGNNV replication in Topics: Animals; Capsid Proteins; Fish Diseases; Fish Proteins; Fishes; HEK293 Cells; Humans; Interferon Regulatory Factors; Interferons; Necrosis; Nodaviridae; RNA Virus Infections; Tretinoin	2022
Excess Retinoic Acid Induces Fusion of Centra by Degenerating Intervertebral Ligament Cells in Japanese flounder, Paralichthys olivaceus. Journal of experimental zoology. Part B, Molecular and developmental evolution, 2016, Volume: 326, Issue:8 In marine aquaculture fish, excessive supplement of vitamin A (VA) to zooplanktons for larval culture and experimental exposure of larvae to retinoic acid (RA: active form of VA) have been known to cause vertebral deformity. However, the tissues in the developing vertebral column that are affected by RA and the progression of vertebral deformity remain undetermined. To examine these questions, we histologically traced the progress of vertebral deformity induced by RA in Japanese flounder (Paralichthys olivaceus). Larvae were exposed to RA for 3 days at mid-metamorphosis (G-stage), a critical stage for vertebral deformity. Intervertebral ligament, which is known to form intervertebral joints in cooperation with the notochord, was severely degenerated by RA, leading to fusion of centra. During further development to adult, growth of centra was severely suppressed in an anterior-posterior direction in RA-treated fish and the notochord tissue was lost from fused centra, resulting in complete loss of intervertebral joints and fusion of centra. We conclude that RA initially damages the intervertebral ligaments, and these defects lead to fusion, narrowing of centra, and loss of intervertebral joints in the vertebral column. The cumulative effect of these modifications is a truncated body form. Topics: Animal Feed; Animals; Bone Development; Dose-Response Relationship, Drug; Fish Diseases; Flounder; Gene Expression Regulation, Developmental; Larva; Ligaments; Spine; Tretinoin	2016

Article

Year

The Capsid Protein of Nervous Necrosis Virus Antagonizes Host Type I IFN Production by a Dual Strategy to Negatively Regulate Retinoic Acid-Inducible Gene-I-like Receptor Pathways.

Journal of immunology (Baltimore, Md. : 1950), 2022, 07-15, Volume: 209, Issue:2

Nervous necrosis virus (NNV), a highly pathogenic RNA virus, is a major pathogen in the global aquaculture industry. To efficiently infect fish, NNV must evade or subvert the host IFN for their replication; however, the precise mechanisms remain to be elucidated. In this study, we reported that capsid protein (CP) of red-spotted grouper NNV (RGNNV) suppressed the IFN antiviral response to promote RGNNV replication in

Topics: Animals; Capsid Proteins; Fish Diseases; Fish Proteins; Fishes; HEK293 Cells; Humans; Interferon Regulatory Factors; Interferons; Necrosis; Nodaviridae; RNA Virus Infections; Tretinoin

2022

Excess Retinoic Acid Induces Fusion of Centra by Degenerating Intervertebral Ligament Cells in Japanese flounder, Paralichthys olivaceus.

Journal of experimental zoology. Part B, Molecular and developmental evolution, 2016, Volume: 326, Issue:8

In marine aquaculture fish, excessive supplement of vitamin A (VA) to zooplanktons for larval culture and experimental exposure of larvae to retinoic acid (RA: active form of VA) have been known to cause vertebral deformity. However, the tissues in the developing vertebral column that are affected by RA and the progression of vertebral deformity remain undetermined. To examine these questions, we histologically traced the progress of vertebral deformity induced by RA in Japanese flounder (Paralichthys olivaceus). Larvae were exposed to RA for 3 days at mid-metamorphosis (G-stage), a critical stage for vertebral deformity. Intervertebral ligament, which is known to form intervertebral joints in cooperation with the notochord, was severely degenerated by RA, leading to fusion of centra. During further development to adult, growth of centra was severely suppressed in an anterior-posterior direction in RA-treated fish and the notochord tissue was lost from fused centra, resulting in complete loss of intervertebral joints and fusion of centra. We conclude that RA initially damages the intervertebral ligaments, and these defects lead to fusion, narrowing of centra, and loss of intervertebral joints in the vertebral column. The cumulative effect of these modifications is a truncated body form.

Topics: Animal Feed; Animals; Bone Development; Dose-Response Relationship, Drug; Fish Diseases; Flounder; Gene Expression Regulation, Developmental; Larva; Ligaments; Spine; Tretinoin

2016