coding sequences cds of crispld2 (Biotechnology Information)

Biotechnology Information coding sequences cds of crispld2

<t>CRISPLD2</t> expression was decreased in severely degenerative NPCs and correlates with patient pain severity. (A) Representative MRI, SOFG, and ACAN IHC staining of NP tissues at Pfirrmann grades II–V. Progressive loss of disc height and matrix components was observed with increasing degeneration. Scale bars: 100 µm (SOFG), 200 µm (ACAN). (B) IF staining of CRISPLD2 in NP samples showing decreased CRISPLD2‐positive cells in severely degenerated tissues. Scale bar: 100 µm. (C) Western blot analysis of CRISPLD2 protein level in NP tissues across degeneration stages and corresponding quantification. (D) The RT‐qPCR analysis showing relative mRNA expression of CRISPLD2 in grades II–V. (E) Pearson correlation between CRISPLD2 expression and patient‐reported VAS pain scores. (F) H&E and SOFG staining of disc sections from sham and LSI mouse. Scale bar: 500 µm. (G) IF staining of Crispld2, Acan, and Mmp3 in sham and LSI model. Scale bar: 500 µm. (H) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (I) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and LSI model. (J) H&E and SOFG staining of disc sections from sham and CINS mouse. Scale bar: 500 µm. (K) IF staining of Crispld2, Acan, and Mmp3 in sham and CINS model. Scale bar: 500 µm. (L) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (M) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and CINS model. Data are presented as mean ± standard deviation (SD), n = 5. Statistical analysis was performed using one‐way ANOVA followed by Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

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CRISPLD2 expression was decreased in severely degenerative NPCs and correlates with patient pain severity. (A) Representative MRI, SOFG, and ACAN IHC staining of NP tissues at Pfirrmann grades II–V. Progressive loss of disc height and matrix components was observed with increasing degeneration. Scale bars: 100 µm (SOFG), 200 µm (ACAN). (B) IF staining of CRISPLD2 in NP samples showing decreased CRISPLD2‐positive cells in severely degenerated tissues. Scale bar: 100 µm. (C) Western blot analysis of CRISPLD2 protein level in NP tissues across degeneration stages and corresponding quantification. (D) The RT‐qPCR analysis showing relative mRNA expression of CRISPLD2 in grades II–V. (E) Pearson correlation between CRISPLD2 expression and patient‐reported VAS pain scores. (F) H&E and SOFG staining of disc sections from sham and LSI mouse. Scale bar: 500 µm. (G) IF staining of Crispld2, Acan, and Mmp3 in sham and LSI model. Scale bar: 500 µm. (H) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (I) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and LSI model. (J) H&E and SOFG staining of disc sections from sham and CINS mouse. Scale bar: 500 µm. (K) IF staining of Crispld2, Acan, and Mmp3 in sham and CINS model. Scale bar: 500 µm. (L) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (M) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and CINS model. Data are presented as mean ± standard deviation (SD), n = 5. Statistical analysis was performed using one‐way ANOVA followed by Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: CRISPLD2 expression was decreased in severely degenerative NPCs and correlates with patient pain severity. (A) Representative MRI, SOFG, and ACAN IHC staining of NP tissues at Pfirrmann grades II–V. Progressive loss of disc height and matrix components was observed with increasing degeneration. Scale bars: 100 µm (SOFG), 200 µm (ACAN). (B) IF staining of CRISPLD2 in NP samples showing decreased CRISPLD2‐positive cells in severely degenerated tissues. Scale bar: 100 µm. (C) Western blot analysis of CRISPLD2 protein level in NP tissues across degeneration stages and corresponding quantification. (D) The RT‐qPCR analysis showing relative mRNA expression of CRISPLD2 in grades II–V. (E) Pearson correlation between CRISPLD2 expression and patient‐reported VAS pain scores. (F) H&E and SOFG staining of disc sections from sham and LSI mouse. Scale bar: 500 µm. (G) IF staining of Crispld2, Acan, and Mmp3 in sham and LSI model. Scale bar: 500 µm. (H) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (I) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and LSI model. (J) H&E and SOFG staining of disc sections from sham and CINS mouse. Scale bar: 500 µm. (K) IF staining of Crispld2, Acan, and Mmp3 in sham and CINS model. Scale bar: 500 µm. (L) Quantification of fluorescence intensity of Crispld2, Acan, and Mmp3. (M) RT‐qPCR analyses of Crispld2 , Acan , and Mmp3 expression in NP tissues from sham and CINS model. Data are presented as mean ± standard deviation (SD), n = 5. Statistical analysis was performed using one‐way ANOVA followed by Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The coding sequences (CDS) of CRISPLD2 (GenBank ID: M679414.1) and IL17A (GenBank ID: OM794745.1 ) were retrieved from the National Center for Biotechnology Information ( https://www.ncbi.nlm.nih.gov/ ).

Techniques: Expressing, Immunohistochemistry, Staining, Western Blot, Quantitative RT-PCR, Fluorescence, Standard Deviation

Crispld2 deficiency exacerbates IVDD and associated pain‐like behaviors. (A) Representative H&E and SOFG staining of lumbar discs from the Crispld2 fl/fl and Crispld2 ‐cKO mice. Histological scores were significantly elevated in Crispld2 ‐cKO discs. Scale bar: 500 µm. (B) IF staining of Acan and Mmp3 in lumbar disc sections. Quantification of fluorescence intensity indicates decreased Acan and increased Mmp3 in Crispld2 ‐cKO discs. Scale bar: 500 µm. (C) Representative MRI images and corresponding Pfirrmann grading show reduced T2‐weighted signal intensity and increased degeneration scores in Crispld2 ‐cKO discs lumbar discs. (D) Western blot analysis of lumbar disc tissue. (E) IF staining of primary NPCs from the Crispld2 fl/fl and Crispld2 ‐cKO discs mice. Scale bar: 50 µm. (F) H&E and SOFG staining of coccygeal discs in the Crispld2 fl/fl and Crispld2 ‐cKO mice. Scale bar: 500 µm. (G) IF of coccygeal discs. Scale bar: 500 µm. (H) MRI imaging and Pfirrmann scores of coccygeal discs. (I) Western blot analysis of coccygeal discs recapitulates lumbar findings. (J) IF of primary NPCs from coccygeal discs. Scale bar: 50 µm. (K) Behavioral analysis across 2‐, 10‐, and 18‐month‐old mice. Data are presented as mean ± SD ( n = 5). Statistical comparisons were performed using unpaired two‐tailed Student's t ‐test or one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: Crispld2 deficiency exacerbates IVDD and associated pain‐like behaviors. (A) Representative H&E and SOFG staining of lumbar discs from the Crispld2 fl/fl and Crispld2 ‐cKO mice. Histological scores were significantly elevated in Crispld2 ‐cKO discs. Scale bar: 500 µm. (B) IF staining of Acan and Mmp3 in lumbar disc sections. Quantification of fluorescence intensity indicates decreased Acan and increased Mmp3 in Crispld2 ‐cKO discs. Scale bar: 500 µm. (C) Representative MRI images and corresponding Pfirrmann grading show reduced T2‐weighted signal intensity and increased degeneration scores in Crispld2 ‐cKO discs lumbar discs. (D) Western blot analysis of lumbar disc tissue. (E) IF staining of primary NPCs from the Crispld2 fl/fl and Crispld2 ‐cKO discs mice. Scale bar: 50 µm. (F) H&E and SOFG staining of coccygeal discs in the Crispld2 fl/fl and Crispld2 ‐cKO mice. Scale bar: 500 µm. (G) IF of coccygeal discs. Scale bar: 500 µm. (H) MRI imaging and Pfirrmann scores of coccygeal discs. (I) Western blot analysis of coccygeal discs recapitulates lumbar findings. (J) IF of primary NPCs from coccygeal discs. Scale bar: 50 µm. (K) Behavioral analysis across 2‐, 10‐, and 18‐month‐old mice. Data are presented as mean ± SD ( n = 5). Statistical comparisons were performed using unpaired two‐tailed Student's t ‐test or one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Staining, Fluorescence, Western Blot, Imaging, Two Tailed Test

Crispld2 deficiency promotes ferroptosis and mitochondrial oxidative stress in NPCs. (A) Quantification of oxidative stress indicators in Crispld2 fl/fl and Crispld2 ‐cKO NPCs, including GSH, GSSG, GSH/GSSG, NADPH, and MDA. (B) Western blot analysis of 4HEN Crispld2 fl/fl and Crispld2 ‐cKO NPCs. (C) TEM of mitochondria in NPCs from Crispld2 fl/fl and Crispld2 ‐cKO mice. Red arrows indicate damaged mitochondria. Scale bar: 50 nm. (D) Representative fluorescence images of intracellular ROS, mitochondrial ROS (MitoSOX), and FerroOrange in Crispld2 fl/fl and Crispld2 ‐cKO NPCs. Scale bar: 20 µm. (E) Representative fluorescence images of Lipid peroxidation in Crispld 2 fl/fl and Crispld2 ‐cKO NPCs. Scale bar: 20 µm. (F) Quantification of fluorescence intensity. (G) Western blot analysis of ferroptosis‐related markers in Crispld2 fl/fl and Crispld2 ‐cKO NPCs. (H) Representative immunofluorescence images and quantification of Gpx4, Acsl4, and Fth. Scale bar: 50 µm. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using two‐tailed unpaired Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: Crispld2 deficiency promotes ferroptosis and mitochondrial oxidative stress in NPCs. (A) Quantification of oxidative stress indicators in Crispld2 fl/fl and Crispld2 ‐cKO NPCs, including GSH, GSSG, GSH/GSSG, NADPH, and MDA. (B) Western blot analysis of 4HEN Crispld2 fl/fl and Crispld2 ‐cKO NPCs. (C) TEM of mitochondria in NPCs from Crispld2 fl/fl and Crispld2 ‐cKO mice. Red arrows indicate damaged mitochondria. Scale bar: 50 nm. (D) Representative fluorescence images of intracellular ROS, mitochondrial ROS (MitoSOX), and FerroOrange in Crispld2 fl/fl and Crispld2 ‐cKO NPCs. Scale bar: 20 µm. (E) Representative fluorescence images of Lipid peroxidation in Crispld 2 fl/fl and Crispld2 ‐cKO NPCs. Scale bar: 20 µm. (F) Quantification of fluorescence intensity. (G) Western blot analysis of ferroptosis‐related markers in Crispld2 fl/fl and Crispld2 ‐cKO NPCs. (H) Representative immunofluorescence images and quantification of Gpx4, Acsl4, and Fth. Scale bar: 50 µm. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using two‐tailed unpaired Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Techniques: Western Blot, Fluorescence, Immunofluorescence, Two Tailed Test

Downregulation of CRISPLD2 activates IL17A signaling pathway in NPCs. (A) PCA showing distinct clustering of transcriptomic profiles between si‐NC and si‐ CRISPLD2 groups. (B) Volcano plot illustrating DEGs between groups. (C) GO enrichment analysis of DEGs. (D) KEGG pathway enrichment of DEGs. (E) GSEA confirming IL17 signaling, cytokine‐mediated signaling, and inflammatory response regulation. (F,G) Western blot and RT‐qPCR analysis showing increased IL17A protein and mRNA levels in si‐ CRISPLD2 versus si‐NC groups. (H) Immunofluorescence staining and quantification of IL17A. Scale bar: 50 µm. (I,J) Western blot and RT‐qPCR analyses showing decreased IL17A expression in CRISPLD2 ‐overexpressing cells. (K) Immunofluorescence staining showing decreased IL17A fluorescence intensity in over‐ CRISPLD2 group. Scale bar: 50 µm. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using unpaired two‐tailed Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: Downregulation of CRISPLD2 activates IL17A signaling pathway in NPCs. (A) PCA showing distinct clustering of transcriptomic profiles between si‐NC and si‐ CRISPLD2 groups. (B) Volcano plot illustrating DEGs between groups. (C) GO enrichment analysis of DEGs. (D) KEGG pathway enrichment of DEGs. (E) GSEA confirming IL17 signaling, cytokine‐mediated signaling, and inflammatory response regulation. (F,G) Western blot and RT‐qPCR analysis showing increased IL17A protein and mRNA levels in si‐ CRISPLD2 versus si‐NC groups. (H) Immunofluorescence staining and quantification of IL17A. Scale bar: 50 µm. (I,J) Western blot and RT‐qPCR analyses showing decreased IL17A expression in CRISPLD2 ‐overexpressing cells. (K) Immunofluorescence staining showing decreased IL17A fluorescence intensity in over‐ CRISPLD2 group. Scale bar: 50 µm. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using unpaired two‐tailed Student's t ‐test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Western Blot, Quantitative RT-PCR, Immunofluorescence, Staining, Expressing, Fluorescence, Two Tailed Test

CRISPLD2 inhibits ferroptosis in NPCs by suppressing IL‐17A–mediated lipid peroxidation and oxidative stress. (A) Schematic representation of experimental groups: (1) si‐NC; (2) si‐ CRISPLD2 ; (3) si‐ CRISPLD2 + si‐ IL17A ; and (4) si‐ CRISPLD2 + IL‐17A inhibitor. (B–F) Biochemical assessment of ferroptosis‐associated redox balance. (G) Representative fluorescence images of FerroOrange, ROS, and MitoSOX staining. Scale bar: 20 µm. (H) Immunofluorescence analysis of lipid peroxidation states. Scale bar: 20 µm. (I) TEM of mitochondria. Red arrows indicate damaged mitochondria, characterized by darker matrix and loss of cristae. Green arrows indicate partially restored mitochondrial cristae. Scale bar: 50 nm. (J,K) Analysis of loading S‐plot (OPLS‐DA). (L,M) Heatmaps of oxidized phosphatidylethanolamine (PE) species and other lipid classes. (N,O) Quantification of PE (18:0/20:4) and PE (18:0/22:4) levels. Data represent mean ± SD ( n = 3). Statistical comparisons were performed using one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: CRISPLD2 inhibits ferroptosis in NPCs by suppressing IL‐17A–mediated lipid peroxidation and oxidative stress. (A) Schematic representation of experimental groups: (1) si‐NC; (2) si‐ CRISPLD2 ; (3) si‐ CRISPLD2 + si‐ IL17A ; and (4) si‐ CRISPLD2 + IL‐17A inhibitor. (B–F) Biochemical assessment of ferroptosis‐associated redox balance. (G) Representative fluorescence images of FerroOrange, ROS, and MitoSOX staining. Scale bar: 20 µm. (H) Immunofluorescence analysis of lipid peroxidation states. Scale bar: 20 µm. (I) TEM of mitochondria. Red arrows indicate damaged mitochondria, characterized by darker matrix and loss of cristae. Green arrows indicate partially restored mitochondrial cristae. Scale bar: 50 nm. (J,K) Analysis of loading S‐plot (OPLS‐DA). (L,M) Heatmaps of oxidized phosphatidylethanolamine (PE) species and other lipid classes. (N,O) Quantification of PE (18:0/20:4) and PE (18:0/22:4) levels. Data represent mean ± SD ( n = 3). Statistical comparisons were performed using one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Techniques: Fluorescence, Staining, Immunofluorescence

CRISPLD2 regulates IL‐17A expression through miR‐548I‐mediated post‐transcriptional suppression. (A) Pie charts showing the distribution of small RNA species in si‐NC and si‐ CRISPLD2 groups. (B) Heatmap illustrating differentially expressed miRNAs upon CRISPLD2 knockdown. (C) KEGG pathway enrichment of differentially expressed miRNAs highlights the IL‐17 signaling pathway and ferroptosis as significantly impacted. (D) RT‐qPCR validation of selected miRNAs shows reduced miR‐548I expression following CRISPLD2 knockdown. (E) Overexpression of CRISPLD2 significantly upregulates miR‐548I expression. (F) Predicted binding site of miR‐548I in the 3'‐UTR of IL‐17A mRNA, indicating direct interaction potential. (G) Dual‐luciferase reporter assay confirms that miR‐548I reduces IL‐17A 3'‐UTR luciferase activity in WT constructs, but not in MUT constructs. (H) Western blot and quantification of IL‐17A protein expression in NPCs co‐treated with si‐ CRISPLD2 and/or miR‐548I mimic. (I) Western blot showing that CRISPLD2 overexpression suppresses IL‐17A, whereas miR‐548I inhibitor rescues IL‐17A expression. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using one‐way ANOVA followed by Tukey's post hoc test or unpaired two‐tailed Student's t ‐test as appropriate. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: CRISPLD2 regulates IL‐17A expression through miR‐548I‐mediated post‐transcriptional suppression. (A) Pie charts showing the distribution of small RNA species in si‐NC and si‐ CRISPLD2 groups. (B) Heatmap illustrating differentially expressed miRNAs upon CRISPLD2 knockdown. (C) KEGG pathway enrichment of differentially expressed miRNAs highlights the IL‐17 signaling pathway and ferroptosis as significantly impacted. (D) RT‐qPCR validation of selected miRNAs shows reduced miR‐548I expression following CRISPLD2 knockdown. (E) Overexpression of CRISPLD2 significantly upregulates miR‐548I expression. (F) Predicted binding site of miR‐548I in the 3'‐UTR of IL‐17A mRNA, indicating direct interaction potential. (G) Dual‐luciferase reporter assay confirms that miR‐548I reduces IL‐17A 3'‐UTR luciferase activity in WT constructs, but not in MUT constructs. (H) Western blot and quantification of IL‐17A protein expression in NPCs co‐treated with si‐ CRISPLD2 and/or miR‐548I mimic. (I) Western blot showing that CRISPLD2 overexpression suppresses IL‐17A, whereas miR‐548I inhibitor rescues IL‐17A expression. Data are presented as mean ± SD ( n = 3). Statistical comparisons were performed using one‐way ANOVA followed by Tukey's post hoc test or unpaired two‐tailed Student's t ‐test as appropriate. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Techniques: Expressing, Knockdown, Quantitative RT-PCR, Biomarker Discovery, Over Expression, Binding Assay, Luciferase, Reporter Assay, Activity Assay, Construct, Western Blot, Two Tailed Test

Crispld2 overexpression alleviates disc degeneration and pain‐associated behaviors, which are reversed by IL‐17A overexpression in vivo. (A) Schematic timeline of LSI mouse model and AAV administration. (B) Representative MRI images of lumbar intervertebral discs in each group ( n = 5). (C) H&E and SOFG staining in lumbar discs ( n = 5). (D) Representative immunofluorescence images of disc sections stained for Acan, Mmp3, IL17A, and 4HNE. Scale bar: 500 µm (Acan), 50 µm (Mmp3, IL17A, and 4HNE), ( n = 5). (E) Quantitative analysis of Acan, Mmp3, IL17A, and 4HNE protein expression ( n = 5). (F,G) Immunofluorescence staining of primary NPCs isolated from mouse discs for Acan, Mmp3, IL17A, and 4HNE. Scale bar: 50 µm, ( n = 5). (H) Quantification of relative fluorescence intensity for Acan, Mmp3, IL17A, and 4HNE in primary NPCs ( n = 5). (I) RT‐qPCR analysis of mRNA expression of Acan , Col2a1 , Mmp3 , and Adamts5 in NP tissues confirms molecular changes ( n = 3). (J) Behavioral testing of mice, including distance traveled, maximum speed, pressure tolerance, and active time ( n = 5). (K) Schematic summary: CRISPLD2 modulates disc degeneration via the miR‐548I‐IL17A axis to inhibit ferroptosis in NPCs. Data are presented as mean ± SD. Comparisons were performed using one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Journal: Advanced Science

Article Title: CRISPLD2 Attenuates Intervertebral Disc Degeneration by Suppressing Oxidative Stress‐Induced Ferroptosis through the miR‐548I‐IL17A Axis

doi: 10.1002/advs.202516477

Figure Lengend Snippet: Crispld2 overexpression alleviates disc degeneration and pain‐associated behaviors, which are reversed by IL‐17A overexpression in vivo. (A) Schematic timeline of LSI mouse model and AAV administration. (B) Representative MRI images of lumbar intervertebral discs in each group ( n = 5). (C) H&E and SOFG staining in lumbar discs ( n = 5). (D) Representative immunofluorescence images of disc sections stained for Acan, Mmp3, IL17A, and 4HNE. Scale bar: 500 µm (Acan), 50 µm (Mmp3, IL17A, and 4HNE), ( n = 5). (E) Quantitative analysis of Acan, Mmp3, IL17A, and 4HNE protein expression ( n = 5). (F,G) Immunofluorescence staining of primary NPCs isolated from mouse discs for Acan, Mmp3, IL17A, and 4HNE. Scale bar: 50 µm, ( n = 5). (H) Quantification of relative fluorescence intensity for Acan, Mmp3, IL17A, and 4HNE in primary NPCs ( n = 5). (I) RT‐qPCR analysis of mRNA expression of Acan , Col2a1 , Mmp3 , and Adamts5 in NP tissues confirms molecular changes ( n = 3). (J) Behavioral testing of mice, including distance traveled, maximum speed, pressure tolerance, and active time ( n = 5). (K) Schematic summary: CRISPLD2 modulates disc degeneration via the miR‐548I‐IL17A axis to inhibit ferroptosis in NPCs. Data are presented as mean ± SD. Comparisons were performed using one‐way ANOVA with Tukey's post hoc test. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001, ns = not significant.

Techniques: Over Expression, In Vivo, Staining, Immunofluorescence, Expressing, Isolation, Fluorescence, Quantitative RT-PCR

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