In the original publication [1], there was a discrepancy in the citation order of the references, starting from reference [87]. The “Chaves, G.; Jardin, C.; Franzen, A.; Mahorivska, I.; Musset, B.; Derst, C. Proton channels in molluscs: A new bivalvian-specific minimal HV4 channel. FEBS J. 2023, 290, 3436–3447. https://doi.org/10.1111/febs.16751.” was missing from the reference list and has now been added as reference 126.
A correction has been made to Table 1, where “Hcl” has been modified to “hcl” for the cell type THP-1.
Table 1.
HV1 in human tissue and other mammalian tissue.
Table 1.
HV1 in human tissue and other mammalian tissue.
| Respiratory Burst | Cell Type | Function of HV1 | References |
|---|---|---|---|
| Yes | Eosinophil (human) (rodent) | Charge compensation, prevention of cell death. | [10,12,17,36–46] |
| Yes | Neutrophil (human) PLB-985 (hcl) HL-60 (hcl) K-562 (hcl) Neutrophil (rodent) | Charge compensation, migration, granula release, calcium homeostasis, pH homeostasis, ERK activity, phagosomal pH homeostasis. | [6,8,10,12–15,41,45,47–53] |
| Yes | Monocyte (human) | Charge compensation. | [54] |
| Yes, small | Macrophage (human) THP-1 (hcl) Macrophage (mice) | Charge compensation, phagosome acidification. | [52,55,56] |
| Yes, small | Osteoclast (rodent/Leporidae) | pH homeostasis, charge compensation, ROS production. | [57–61] |
| Yes, small | Microglia (rodent) Microglia culture (human) BV-2 (rcl) GM1-R1 (rcl) MLS-9 (rcl) | pH homeostasis, charge compensation, ROS production, microglia-astrocyte communication, neuropathic pain promotion, brain damage enhancing, acidosis exacerbation, M2 polarization reduction, demyelination promotion, white matter injuries promotion, secondary spinal cord damage enhancing, neuroinflammation promotion, pyroptosis increase, motor deficit expansion, autophagy increase, M1 polarization promotion in aged mice. | [22,61–77] |
| Yes | Kupffer cell (mice/rodent) | Glucose metabolism, ROS production suppression, hyperglycaemia, and hyperinsulinemia prevention. | [23] |
| No | Cardiac fibroblast (human) | pH homeostasis, membrane potential, potentially beneficial in ischemia. | [78] |
| Yes, small | Dendritic cells (rodent/human) | TLR9 activation. | [28] |
| No | Sperm cell (human) | Capacitation, acid extrusion. | [32,33,79,80] |
| Yes | Oocyte (human) | pH homeostasis. | [34] |
| No | Type 2 alveolar cells (rodent) | pH regulation. | [5,30,47,81–87] |
| No | Mast cell (mouse) | pH homeostasis. | [88] |
| Yes, tiny | B cells (human) (rodent) LK35.2 (rodent) | B cell receptor signalling, migration and proliferation enhancing (short isoform). | [26,27,89,90] |
| No | T cells (human) Jurkat (human) T cells (rodent) | Apoptosis prevention, pH homeostasis, autoimmune disorders prevention. | [29,89,91–93] |
| No | Cardiomyocytes (canine) | pH homeostasis. | [11] |
| No | SHG-44 glioma cells (human) | Apoptosis prevention. | [18] |
| No | Colorectal cancer (human) SW620 (hcl) HT29 (hcl) LS174T (hcl) Colo205 (hcl) | Prevention of cellular acidosis, support of cancer cell metabolism, pH homeostasis, potential biomarker, and drug target. | [19] |
| No | Basophils (human) | Exocytosis (histamine release), pH homeostasis. | [16,94] |
| No | Ovary cells (Hamster) | pH homeostasis. | [95] |
| No | Breast cancer cells (human primary) MDA-BA-231(hcl) MCF-7 (hcl) MDA-MB-468 (hcl) MDA-MB-453 (hcl) T-47D (hcl) SK-BR-3 (hcl) | Tumor growth, metastasis and invasiveness promotion, (expression predicts prognosis of tumor). | [20,21,96] |
| No | Lung cancer cell A549 (human) | No information. | [97] |
| No | Prostate cancer cell PC-3 (human) | No information. | [97] |
| No | Kidney (human) HEK-293 | No information. | [97,98] |
| Yes, small | Nasal epithelium (human primary culture) JME/CF 15 (human) Cystic fibrosis genotype | Airway surface epithelium acidification, proton extrusion. | [99] |
| Yes, small | Ciliated tracheal cells (human) | NADPH oxidase activity driven proton extrusion. | [31,99] |
| Yes, small | lung epithelium fetal (human) | DUOX driven proton release, acid extrusion. | [100] |
| Yes, tiny | Serous gland cell line Calu-3 (human) | Airway surface epithelium acidification, proton extrusion (to a lesser extent than airway epithelium). | [31] |
| No | Skeletal muscle myocyte (human) | pH homeostasis. | [7] |
| No | Glioblastoma cell line (human) T98G | Cell’s survival and migration. | [101] |
| No | Whole heart (rodent) | NOXs transcription and CO2 homeostasis control, electrophysiological remodelling. | [102] |
| No/Yes | Vascular system, Immune system | Atherosclerosis advancement (hypothetical). | [103] |
| No/Yes Whole tissue | Lung (rodent) | Goblet cell hyperplasia prevention. Depression expression of IL-4, IL-5, and IL-13. Reduction of the expression levels of NOX2, NOX4, and DUOX1. Promotion of the expression of SOD2 and catalase. Reduction of the development of allergic asthma through ROS production enhancing. | [104] |
| Yes | Myeloid derived suppressor cells (MDSC) (rodent) | T-cells regulation (via ROS production). | [35] |
| No | epididymal adipose tissue (rodent) | Diet obesity induction. | [24] |
| Yes, tiny | Pancreatic β cells (rodent) | Insulin secretion, ROS production, NOX4 upregulation, glucotoxicity induction. | [25,105,106] |
hcl = human cell line; rcl = rodent cell line.
In Table 4, letter designations for “a,b,c,e,c” were incorrectly assigned. These designations have been corrected throughout the table to ensure proper attribution.
Table 4.
Biophysical properties of some HV channels.
Table 4.
Biophysical properties of some HV channels.
| Organism | Species | Channel | Oligomerization? | Selectivity | Gating Charges, e0 | Slope Vthres/Vrev | Vthres at ΔpH = 0 (mV) | ΔgH-V/ΔpH (mV/pHo) | H+ Influx at Relevant Physiological pH? | References |
|---|---|---|---|---|---|---|---|---|---|---|
| Mammals | H. sapiens | hHV1 | confirmed f,g,j,k | >106 PH+/PTMA+ e,i >106 PH+/PCH3SO3- i >106 PH+/PCl- i | ~5 h,δ ~6 l | 0.82 e 0.67–0.71 (expressed) l 0.71 (native) l | 13.8 e −9 to −11 (expressed) l +27 (native) l | 40 l | no (native) yes (if expressed) l | [111] e, [139] f, [140] g, [141] h, [142] i, [41] j, [143] k, [98] l |
| M. musculus | mHV1 | confirmed n | >107 PH+/PNMDG+ >107 PH+/PNa+ >107 PH+/PK+ | ~6 m | 0.86 * (expressed) 0.69 m (expressed) | +10 to +20 −15 (expressed) m | 50 40 m | no (native) yes (if expressed) m | [119], [98] m, [144] n | |
| R. norvegicus | RnHV1 | possibly | >107 PH+/PTMA+ o >108 PD+/PTMA+ p | 5.4 p | 0.76 | +18 | 44 40 o,p | no | [5], [81] o, [83] p | |
| Fish | D. rerio | DrHV1 | possibly | >107 PH+/PNMDG+ | n.d. | 0.69 * | ~+10 mV ε | ~40 ε | no | [145] |
| Sea squirt | C. intestinalis | CiHV1 | confirmed c | n.d. | 4.4–5.9 (dimer) c 1.6–2.7 (monomer) d | n.d. | n.d. | ~40 d | no | [119], [146] c, [147] d |
| Insects | N. phytophila | NpHV1 | confirmed b | >108 PH+/PTMA+ >104 PH+/PNa+ >104 PH+/PCl- | 4.7–6.1 b | 0.81 a | −3.4 a | 47–54 a | no | [121] a, [148] b |
| E. tiaratum | EtHV1 | n.d. | >106 PH+/PTMA+ | n.d. | 0.77 | −23 | 45 | yes | [122] | |
| Mollusks | C. gigas | CgHV4 | possibly | >107 PH+/PTMA+ | n.d. | 0.84 | −12 | 49 | no ● | [126] |
| A. californica | AcHV1 | possibly | >107 PH+/PTMA+ >106 PH+/PNa+ >106 PH+/PK+ | 5.7 | 0.78 | 5 | 43–45 | no | [125] | |
| A. californica | AcHV2 | possibly | >107 PH+/PTMA+ >106 PH+/PK+ | 5.3 | 0.77 | −20 | 44 40 (pHi) | yes | [125] | |
| A. californica | AcHV3 | possibly + | >107 PH+/PTMA+ | n.d. | n.d. | n.d. | n.d. | yes § | [125] | |
| H. trivolvis | HtHV1 | possibly | >107 PH+/PTMA+ | 5.5 | 1.03 * 0.26 (pHi) * | n.d. | 60.0 15.3 (pHi) | no | [149] | |
| Corals | A. millepora | AmHV1 | confirmed | >107 PH+/PTMA+ | 2 λ | 0.86 * | ~+10 mV θ | ~50 θ | no | [124] |
| Sea Urchin | S. purpuratus | SpHV1 | confirmed | >107 PH+/PK+ | 4.3 (dimer) 1.1 (monomer) | 0.69 * | ~+10 mV | ~40 β | no | [123] |
| Fungi | A. oryzae | AoHV1 | possibly + | >105 PH+/PTEA+ # | 5 | 1.40–1.55 * | ~−30 (pH 5.5) γ ~−30 (pH 6.5) γ | 80–90 | yes | [130] |
| S. luteus | SlHV1 | possibly + | >105 PH+/PTEA+ # | 5 | 1.40–1.55 * | ~+20 (pH 5.5) γ ~+40 (pH 6.5) γ | 80–90 | no | [130] | |
| Dinoflagellates | K. veneficum | kHV1 | possibly not φ | >107 PH+/PTMA+ >105 PH+/PCl- | n.d. | 0.79 | −37 | 46 | yes | [133] |
| L. polyedrum | LpHV1 | possibly + | >109 PH+/PTMA+ | n.d. | 0.69 * | 46 | 40 ** | yes α | [134] | |
| Phytoplankton | E. huxleyi | EhHV1 | possibly | >106 PH+/PK+ >106 PH+/PCl- | n.d. | 0.69 μ (expressed) | ~+20 mV (expressed) μ | ~40 Ω | no | [132] |
| C. pelagicus | CpHV1 | possibly | >106 PH+/PK+ >106 PH+/PCl- | n.d. | 0.69 μ (native) | +10 mV (native) μ | ~40 Ω | no | [132] |
* Calculated from conductance shifts (∆gH-V/∆pH) and EH = 58 mV·pH−1. § AcHV3 leaks protons at the closed state [125]. # Calculated from pH = 6.0 and working solution containing 30 mM of TEA+ as main cation. ● CgHV4 has an activation of −12 mV which permits proton influx at symmetrical pH (physiological) conditions. Nevertheless, the proximity of the offset value to Vrev makes the inward H+ electrochemical gradient small. Thus, H+ influx is small at ∆pH = 0 where currents rectify rapidly with depolarization, behaving more like a typical HV proton extruder. During measurements, strong and/or consistent H+ influx currents were not detected. φ kHV1 lacks the predicted coiled-coil which is important for HV dimerization, a potential monomeric expression is discussed by the authors [133]. + Protein sequence analysis predicts a C-terminal coiled-coil domain. ** LpHV1 pH-dependent gating saturates above pHo 8.0 [134] similar to rat, human, Karlodinium, and Emiliania HV channels [137]. α Inward H+ currents are onset at large inward pH gradients (1–3 ∆pH units) [134]. β estimated from gH-V curves shift between pHo 6.5 and 7.0 (~20 mV), at pHi = 7.0 (Figure 2; [123]). The gH-V shifts between pHo 6.0 to 6.5 and 6.5 to 7.0 are not identical due to experimental limitations reported by the authors. The calculated value on pHo-dependent gating agrees with ΔgH-V/pHi unit (Figure S1; [123]). γ from normalized gH-V curves (Figure 3; [130]). δ from Qon of dimeric W207A-N214R mutant ([141]). θ from Vthres-ΔpH and slope of V0.5-ΔpH curves (Figure 6; [124]). λ apparent from steepness of normalized gH-V (Figure 6; [124]). Ω from current densities (Figure 1; [132]). μ the slope Vthres/Vrev was calculated from shifts of IH onsets and EH. Voffset was estimated shifts of IH activation, EH, and Equation (3) (Figure 4; [132]). PH+ = proton permeability, PTMA+ = tetramethylammonium permeability, PTEA+ = tetraethylammonium permeability, PK+ = potassium permeability, PNa+ = sodium permeability, PCl- = chloride permeability, PNMDG+ = N-methyl-d-glucamine permeability, PCH3SO3-= methanesulfonate permeability, n.d. = no data, Vthres = threshold potential, Vrev = reversal potential, ∆pH = proton gradient (pHoutside – pHinside), gH-V = proton conductance – voltage relationship, pHo = external pH, pHi = internal pH.
Additionally, several textual clarifications have been made: the term “putatively” was added to qualify the described mechanism, the phrase “translate to” was introduced to improve the accuracy of the affected sentence, and the repeated year “2006” in the description of the Ciona intestinalis homolog was removed.
With this correction, the order of some references has been adjusted accordingly. The authors state that the scientific conclusions are unaffected. This correction was approved by the Academic Editor. The original publication has also been updated.
Reference
- Chaves, G.; Jardin, C.; Derst, C.; Musset, B. Voltage-Gated Proton Channels in the Tree of Life. Biomolecules 2023, 13, 1035. [Google Scholar] [CrossRef] [PubMed]
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