cd38  (R&D Systems)

Journal: Materials Today Bio

Article Title: Injectable antifibrotic drug-loaded hydrogels reduce fibrosis and restore myogenesis by enhancing mitochondrial metabolism and cell mechanics in an in vitro coculture model

doi: 10.1016/j.mtbio.2026.103033

Figure Lengend Snippet: Establishment and characterization of a fibrotic macrophage-muscle fibrosis model. a) Brightfield image of unstimulated RAW264.7 cells in the top chamber of a RAW-C2C12 coculture system, b) Brightfield image of C2C12 cells in the bottom chamber under basal coculture conditions, c) Fluorescence image of C2C12 cells in the bottom chamber exhibiting myotube morphology, d) Fluorescence image confirming the absence of fibrotic marker expression in C2C12 cells under basal conditions, e) Brightfield image of LPS-activated RAW264.7 cells in the top chamber, f) Brightfield image of C2C12 cells in the bottom chamber displaying a myofibroblast-like morphology post-LPS activation, g) Fluorescence image of phenotypic transition of C2C12 cells to myofibroblast-like cells, h) Fluorescence image demonstrating fibrotic protein expression in LPS-treated C2C12 cells (magenta arrow indicates CD38 cells). Immunostaining images: In panels c) and g), TGF-β, DAPI, and actin are colored red, blue, and green, respectively. In panels d) and h), COL1, α-SMA, CD38, and DAPI are colored red, blue, magenta, and green, respectively. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)

Article Snippet: Mouse monoclonal antibodies against myosin heavy chain (MyHC), CD38, and transforming growth factor-β (TGF-β), as well as rabbit polyclonal α-smooth muscle actin (α-SMA) antibodies, were purchased from R&D Systems (USA).

Techniques: Fluorescence, Marker, Expressing, Activation Assay, Immunostaining

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: CD38 expression and activity increase at late stages of ZIKV infection and correlate with NAD + decline in the brain (A) Total NADase activity measured in the brains of ZIKV-infected and mock-injected mice over the course of infection, showing significant increases from 18 dpi onward ( n ≥ 7 mice per group). (B) Overlay of NADase activity (red line) and NAD + levels (gray line), both relative to mock controls (dashed line), showing an inverse temporal association. (C–H) Relative mRNA expression of Sarm1 , Cd157 , and Cd38 , respectively, in the brains of ZIKV-infected and control mice ( n ≥ 4 mice per group). (D, F, H) Overlays of mRNA expression profiles of Sarm1 (D), Cd157 (F), and Cd38 (H) with NAD + levels (gray line) and ZIKV genomic RNA (yellow line), indicating that Cd38 induction temporally coincides with NAD + decline, while Sarm1 and Cd157 do not. (I) Linear regression shows a positive correlation between total NADase activity and Cd38 mRNA expression ( n = 50). (J) CD38-dependent NADase activity, calculated as the fraction inhibited by the specific CD38 inhibitor 78c ( n ≥ 6 mice per group). (K) CD38-independent NADase activity, which remains low and unchanged during infection ( n ≥ 6 mice per group). (L) On the right, representative Western blot of CD38 protein expression in brain extracts at 24 dpi, with α-tubulin as loading control (representative bands from the same experiment shown in the full blot in ). On the left, quantification of the Western blot bands’ intensities (CD38/α-tubulin) relative to mock ( n ≥ 4 mice per group). Data in panels A, C, E, G, J, K, and L are presented as mean ± SD; panels B, D, F, and H as mean ± SEM (shaded area). Statistical significance was determined by unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Activity Assay, Infection, Injection, Control, Western Blot, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: CD38 inhibition prevents NAD + depletion in the brains of ZIKV-infected mice (A) Schematic representation of the experimental design. Neonatal mice were subcutaneously infected with ZIKV at postnatal day 3 (P3). At 21 days post-infection (dpi), animals received a unilateral intracerebroventricular (i.c.v.) injection of the CD38-blocking antibody Ab68 (5.76 μg) or vehicle (Veh), and brains were collected at 24 dpi for analysis. (B) NAD + hydrolase activity in brain tissue. (C) Quantification of total NAD + levels in brain tissue. Data are presented as mean ± SD. Statistical analyses were performed using an unpaired Student’s t test ( n ≥ 7 mice per group). ∗p ≤ 0.05; ∗∗∗∗p ≤ 0.0001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Inhibition, Infection, Injection, Blocking Assay, Activity Assay

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: NAMPT is induced in the brain of ZIKV-infected mice (A) Relative mRNA expression of Nampt in the brains of ZIKV-infected and mock-injected mice across time points post-infection ( n ≥ 4 mice per group). (B) Overlay of Nampt mRNA expression (blue line), total NADase activity (red line), NAD + levels (gray line), and ZIKV genomic RNA (yellow line), all relative to mock controls (dashed line). (C–F) Correlation analyses between Nampt mRNA expression and (C) ZIKV genomic RNA, (D) Parp12 , (E) Parp10 , and (F) Cd38 mRNA expression. Nampt shows a strong correlation with viral load and early-induced Parps , but a weak correlation with Cd38 . (G) Representative Western blot of NAMPT protein expression in the brains of ZIKV-infected and mock-injected mice at 24 days post-infection (dpi; representative bands from the same experiment shown in the full blot in ).. HPRT was used as a loading control. The right panel shows quantification of NAMPT protein levels (NAMPT/HPRT ratio), normalized to mock controls ( n ≥ 4 mice per group). Data in panels A and G are presented as mean ± SD; panel B as mean ± SEM (shaded area). Correlations were assessed by linear regression analysis. Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Infection, Expressing, Injection, Activity Assay, Western Blot, Control, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: Proinflammatory cytokine expression precedes CD38 induction in the brains of ZIKV-infected mice (A, C, E) Relative mRNA expression of Il6 and Tnf (linear scale), and Ccl5/Rantes (Log 10 -transformed) in the brains of ZIKV-infected and mock-injected mice across time points post-infection ( n ≥ 3 mice per group). All three inflammatory mediators were significantly upregulated during the early and mid-stages of infection. (B, D, F) Overlay of Il6 (B), Tnf (D), and Rantes – log 10 scale (F) mRNA expression profiles (purple line) with Cd38 mRNA (red line), NAD + levels (gray line), and ZIKV genomic RNA (yellow line), all relative to mock controls (dashed line). (G) Brain IL-6 protein levels determined by ELISA ( n ≥ 5 mice per group). The temporal pattern shows that cytokine and chemokine induction precede Cd38 expression, suggesting that neuroinflammation may contribute to the upregulation of CD38. Data in panels A, C, and E are presented as mean ± SD; panels B, D, and F as mean ± SEM (shaded area). Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗ p ≤ 0.001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Infection, Transformation Assay, Injection, Enzyme-linked Immunosorbent Assay, MANN-WHITNEY

Journal: iScience

Article Title: CD38 is a key mediator of NAD + depletion in the brain of ZIKV-infected mice

doi: 10.1016/j.isci.2025.114018

Figure Lengend Snippet: Infiltrating immune cells contribute to increased CD38 expression in the brains of ZIKV-infected mice (A) On the left, representative dot plots show the gating strategy used to identify CD45 lo CD11b + (putative resting microglia), CD45 hi CD11b + (infiltrating myeloid cells), and CD45 + CD11b − (lymphoid cells) populations. On the right, graphs showing the frequency of each population in ZIKV-infected and mock-injected mice ( n ≥ 5 mice per group). (B) Representative dot plots and quantification of CD11b + TMEM119 + , CD11b + TMEM119 + , and CD11b + TMEM119 - populations in the brains of infected and control mice ( n ≥ 6 mice per group), with the respective graphs showing the frequency of each population. (C–E) Representative histograms and quantification of CD38 expression (median fluorescence intensity, MFI) in CD11b + TMEM119 + (C) CD11b − TMEM119 + (D), and CD11b + TMEM119 - (E) populations. (F and G) Gating and quantification of CD3 + T cells (F) and corresponding CD38 expression (G). (H and I) Gating and quantification of CD19 + B cells (H) and corresponding CD38 expression (I). All graphs represent mean ± SD. Gating was based on negative controls; histogram quantification was performed using MFI, and curves were normalized to unit area. Statistical analyses were performed using an unpaired Student’s t test or Mann–Whitney test, as appropriate. ∗ p ≤ 0.05; ∗∗ p ≤ 0.01; ∗∗∗∗ p ≤ 0.0001.

Article Snippet: Proteins were separated by electrophoresis on 15% SDS–polyacrylamide gels (SDS-PAGE), transferred to nitrocellulose membranes (Bio-Rad, California, USA), and probed with primary antibodies against CD38 (AF4947, R&D Systems, Minnesota, USA) or NAMPT (AG-20A-0034-C050, AdipoGen Life Sciences, California, USA), using concentrations recommended by the manufacturers and previously validated in-house.

Techniques: Expressing, Infection, Injection, Control, Fluorescence, MANN-WHITNEY

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid

doi: 10.1007/s00018-025-05891-7

Figure Lengend Snippet: ALDH1A1 increased after conventional chemotherapy regimen Vrd or Krd. A and B. GSE276561 and GSE47552 datasets revealed ALDH1A1 in MM was lower than healthy control; These GEO data were analyzed by on line tool GEO2R using Benjamini & Hochberg (False discovery rate) method; Each y axis label in the graph represents the expression measurement extracted from the TPM normalized expression counts (for RNA-seq), or the Value column of the original submitter-supplied Sample record (for microarrays). All the y axis label represents normalized mRNA expression level. C. mRNA levels of ALDH1A1 in NDMM samples are significantly lower than healthy control, but remarkably higher in RRMM samples than NDMM patients which are collected in our hospital; Relative ALDH1A1 levels is relative to GAPDH. D. mRNA levels of CD38 in NDMM patients are significantly higher than healthy control which are collected in our hospital; Relative CD38 levels is relative to GAPDH. E. ALDH1A1 mRNA increased after Vrd or Krd treatment; Relative ALDH1A1 levels is relative to GAPDH. F . western blot confirmed ALDH1A1 protein increased after Vrd or Krd treatment. **, p < 0.01, ***, p < 0.001. C-E, Data was analyzed by Mann-Whitnay test HC: healthy control; Vrd: Bortezomib + Lenalidomide + Dexamethasone; KRd: Carfilzomib + Lenalidomide + Dexamethasone; MM: multiple myeloma; NDMM: newly diagnosed multiple myeloma; SMM: smoldering multiple myeloma; MGUS: monoclonal gammopathy of undetermined significance

Article Snippet: The positive CD38 cells were labeled by APC anti-human CD38 antibody (E-AB-F1058E, Elabscience) or APC anti-mouse CD38 antibody (E-AB-F1193E, Elabscience) and analyzed by FACSCantoTM II flow cytometer.

Techniques: Control, Expressing, RNA Sequencing, Western Blot

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid

doi: 10.1007/s00018-025-05891-7

Figure Lengend Snippet: ALDH1A1 down-regulated in the nrRRMM patients received Dara-Rd treatment. A and B. rRRMM patients had higher ALDH1A expression compared with nrRRMM after Dara-Rd treatment analyzed by RT-qPCR and western blot; C and D . the CD38 expression (mRNA and protein) decreased in Dara-treated patients in nrRRMM patients compared with rRRMM patients; E . the mRNA expression of ALDH1A1 after Dara-based treatment was positively correlated with the CD38 mRNA expression. **, p < 0.01 A-D, data was analyzed by student t test. E, data was analyzed by simple linear regression nrRRMM: non-responder relapsed/refractory multiple myeloma; rRRMM: responder relapsed/refractory multiple myeloma; MFI: median fluorescence intensity; Dara-Rd: daratumumab + lenalidomide + dexamethasone; Dara: daratumumab

Article Snippet: The positive CD38 cells were labeled by APC anti-human CD38 antibody (E-AB-F1058E, Elabscience) or APC anti-mouse CD38 antibody (E-AB-F1193E, Elabscience) and analyzed by FACSCantoTM II flow cytometer.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Fluorescence

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid

doi: 10.1007/s00018-025-05891-7

Figure Lengend Snippet: ALDH1A1 directly regulates CD38 expression in H929 cells. A . the KD efficiency of different sh-ALDH1A1 sequences; B . Knock down ALDH1A1 decreased CD38 genes expression; C. Re-introducing ALDH1A1-OE plasmid restored downregulation of ALDH1A1 mRNA levels in ALDH1A1-KD cells; D . Re-introducing ALDH1A1 into ALDH1A1-KD cells significantly upregulate the expression of CD38; E . cell-surface expression of CD38 decreased in ALDH1A1-KD cells but restored by re-introducing ALDH1A1-OE plasmid determined by flow cytometry analysis. **, p < 0.01, ***, p < 0.001 Student t test was performed in all datasets AlDH1A1-KD: ALDH1A1 knockdown; Ctrl: control; shALDH1A1: short hairpin RNA for ALDH1A1; KD-OE: over expression of ALDH1A1 in KD cells

Article Snippet: The positive CD38 cells were labeled by APC anti-human CD38 antibody (E-AB-F1058E, Elabscience) or APC anti-mouse CD38 antibody (E-AB-F1193E, Elabscience) and analyzed by FACSCantoTM II flow cytometer.

Techniques: Expressing, Knockdown, Plasmid Preparation, Flow Cytometry, Control, shRNA, Over Expression

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid

doi: 10.1007/s00018-025-05891-7

Figure Lengend Snippet: ALDH1A1 increased CD38 through activation of RA/RAR via RA production. A . Volcano plots created by differential mRNA (fold change (FC) > 2 or < 0.5, and p < 0.05); B. KEGG analysis in ALDH1A1 KD cells of H929 and 8226 cells revealed that retinoic acid receptor, and retinoid X receptor agonists/antagonists pathways were enriched in both cell line; C. Knock down ALDH1A1caused downregulation of RAR proteins while re-introduced ALDH1A1 into ALDH1A1-KD cells increased their expressions; D . RA salvage restore the ADCC of Dara against MM cells; E . the RAR protein level was significantly increased determined by western blot after RA supplement; (F) mRNA levels of CD38 determined by RT-qPCR; (G) protein levels of CD38 determined by western blot. **, p < 0.01, ***, p < 0.001 C-G, student t test was adopted KD: ALDH1A1 knockdown; Ctrl: control; KD-OE: over expression of ALDH1A1 in KD cells; RA: retinoic acid; RAR: retinoic acid receptor; ADCC: antibody-dependent cellular cytotoxicity

Article Snippet: The positive CD38 cells were labeled by APC anti-human CD38 antibody (E-AB-F1058E, Elabscience) or APC anti-mouse CD38 antibody (E-AB-F1193E, Elabscience) and analyzed by FACSCantoTM II flow cytometer.

Techniques: Activation Assay, Knockdown, Western Blot, Quantitative RT-PCR, Control, Over Expression

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: Reduced ALDH1A1 expression in multiple myeloma cells increases resistance to daratumumab via downregulation of retinoic acid

doi: 10.1007/s00018-025-05891-7

Figure Lengend Snippet: ALDH1A1 inhibitor reduces the sensitivity of Dara in vivo through inhibiting the RA/RAR pathway. A and B . compared with vehicle control, Dara cause significantly reduction of xenograft tumors weight and tumor growth; C . inhibitor of ALDH1A 673 A remarkably reduce the protein level of CD38, ALDH1A1 and RAR, and RA complement significantly restore the protein level of CD38 and RAR. *, p < 0.05, **, p < 0.01, ***, p < 0.001 A-B, analysis of variance (ANOVA) was used for multi-group comparisons followed by Tukey’s post hoc test ( N = 6); C, analysis of variance (ANOVA) was used for multi-group comparisons followed by Tukey’s post hoc test ( N = 3) RA: retinoic acid; RAR: retinoic acid receptor

Article Snippet: The positive CD38 cells were labeled by APC anti-human CD38 antibody (E-AB-F1058E, Elabscience) or APC anti-mouse CD38 antibody (E-AB-F1193E, Elabscience) and analyzed by FACSCantoTM II flow cytometer.

Techniques: In Vivo, Control